Journal articles: 'Mice – Immunology'

1

Wickelgren, I. "Immunology: Muscling Transplants Into Mice." Science 273, no. 5271 (July 5, 1996): 33–0. http://dx.doi.org/10.1126/science.273.5271.33.

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Masopust, David, Christine P. Sivula, and Stephen C. Jameson. "Of Mice, Dirty Mice, and Men: Using Mice To Understand Human Immunology." Journal of Immunology 199, no. 2 (July 10, 2017): 383–88. http://dx.doi.org/10.4049/jimmunol.1700453.

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3

Williams, N. "Immunology: Simple Mice Test Antibody Complexity." Science 272, no. 5268 (June 14, 1996): 1585–0. http://dx.doi.org/10.1126/science.272.5268.1585.

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4

Newman, Kira L., and Juan S. Leon. "Norovirus immunology: Of mice and mechanisms." European Journal of Immunology 45, no. 10 (August 25, 2015): 2742–57. http://dx.doi.org/10.1002/eji.201545512.

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Buqué, Aitziber, and Lorenzo Galluzzi. "Modeling Tumor Immunology and Immunotherapy in Mice." Trends in Cancer 4, no. 9 (September 2018): 599–601. http://dx.doi.org/10.1016/j.trecan.2018.07.003.

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Wilson, Christopher B., Christel H. Uittenbogaart, and Diane J. Mathis. "Immunology at Asilomar: from molecules to mice." Nature Immunology 4, no. 4 (April 2003): 300–302. http://dx.doi.org/10.1038/ni0403-300.

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Bieberich, Charles, and George Scangos. "Transgenic mice in the study of immunology." BioEssays 4, no. 6 (June 1986): 245–48. http://dx.doi.org/10.1002/bies.950040603.

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Kheirouri, Sorayya, and Mohammad Alizadeh. "Experimental immunology Decreased serum and mucosa immunoglobulin A levels in vitamin A- and zinc-deficient mice." Central European Journal of Immunology 2 (2014): 165–69. http://dx.doi.org/10.5114/ceji.2014.43716.

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Wilkes, D. S., K. M. Heidler, L. K. Bowen, W. M. Quinlan, N. A. Doyle, O. W. Cummings, and C. M. Doerschuk. "Allogeneic bronchoalveolar lavage cells induce the histology of acute lung allograft rejection, and deposition of IgG2a in recipient murine lungs." Journal of Immunology 155, no. 5 (September 1, 1995): 2775–83. http://dx.doi.org/10.4049/jimmunol.155.5.2775.

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Abstract The immunologic and histologic changes associated with lung allograft rejection are believed to result from the presentation of donor lung alloantigens to recipient lymphocytes resulting in up-regulated Th1 lymphocyte activity. The ability of allogeneic lung immune cells to induce the pathologic and immunologic changes associated with acute lung allograft rejection are unknown. The current study determined whether allogeneic (C57BL/6, I-a(b)) bronchoalveolar lavage (BAL) cells (> or = 97% macrophages), when instilled into the lungs of recipient BALB/c mice (I-a(d)), induced the histology and immunology associated with acute lung allograft rejection. BALB/c mice received BAL cells from either C57BL/6 mice (allogeneic instillate) or BALB/c mice (autologous instillate) or PBS (control) by nasal insufflation weekly for 4 wk. Allogeneic BAL cells resulted in a lymphocytic bronchitis and vasculitis analogous to grade 1 to 2 lung allograft rejection. The mice given allogeneic instillates had a greater percentage of lymphocytes in the BAL fluid than those given autologous instillates. After instillation of allogeneic BAL cells, the Th1 cytokines, IL-2 and IFN-gamma (IFN-gamma), were produced locally in greater quantities and more frequently than Th2 cytokine IL-10. IL-4, another Th2 cytokine, was not detected. The local production of IgG1 and IgG2a, which are dependent on IL-4 and IFN-gamma, respectively, were increased. However, only IgG2a was deposited in the perivascular and peribronchiolar tissues. These data show that installation of allogeneic BAL cells into the airways of recipient mice induced up-regulated Th1 lymphocyte activity and caused the histologic changes associated with lung allograft rejection.

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Mak, Tak W., Josef M. Penninger, and Pamela S. Ohashi. "Knockout mice: a paradigm shift in modern immunology." Nature Reviews Immunology 1, no. 1 (October 2001): 11–19. http://dx.doi.org/10.1038/3509551.

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Mak, Tak W., Josef M. Penninger, and Pamela S. Ohashi. "KNOCKOUT MICE: A PARADIGM SHIFT IN MODERN IMMUNOLOGY." Nature Reviews Immunology 1, no. 1 (October 2001): 11–19. http://dx.doi.org/10.1038/35095551.

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Lee, David M., Herman F. Staats, John S. Sundy, Dhavalkumar D. Patel, Gregory D. Sempowski, Richard M. Scearce, Dawn M. Jones, and Barton F. Haynes. "Immunologic Characterization of CD7-Deficient Mice." Journal of Immunology 160, no. 12 (June 15, 1998): 5749–56. http://dx.doi.org/10.4049/jimmunol.160.12.5749.

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Abstract Human CD7 is an Ig superfamily molecule that is expressed on mature T and NK lymphocytes. Although in vitro studies have suggested a role for CD7 in lymphoid development and function, the exact function of CD7 in vivo has remained elusive. One patient has been reported with SCID syndrome attributed to CD7 deficiency. To study in vivo functions of CD7, we have generated CD7-deficient mice and assessed their lymphoid development and function. CD7-deficient mice were viable, had normal peripheral blood and spleen lymphocyte numbers, and had normal specific Ab responses with Ag-driven Ig isotype switching. Thymocyte numbers were normal in 4-wk-old, 6-mo-old, and 1-yr-old CD7-deficient mice, but in 3-mo-old CD7-deficient mice, total thymocyte numbers were significantly increased by 60% (p < 0.02) compared with normal age-matched +/+ littermates. CD7-deficient splenocytes proliferated normally in response to various mitogens, including PHA, anti-CD3, Con A, and LPS. While NK cell numbers and cytolytic activity to YAC targets were normal, CD7-deficient mice had lower Ag-induced MHC class I-restricted CTL activity against OVA-transfected target cells than did +/+ control mice. Thus, CD7-deficient mice did not have a SCID syndrome, but rather had transient increases in thymocyte numbers at age 3 mo and altered splenocyte Ag-specific CTL effecter cell activity. These data suggest a role for CD7 in regulating intrathymic T cell development and in mediating CTL effecter function.

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Perez, Jessica, and Derek Abbott. "TNFα-mediated I kappa kinase phosphorylation of ITCH impairs ubiquitin ligase activity (IRM11P.625)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 132.4. http://dx.doi.org/10.4049/jimmunol.194.supp.132.4.

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Abstract The I Kappa Kinase (IKK) signalosome serves as a central hub for the relay of inflammatory signaling. Once activated, the kinase components of this hub, IKKα and IKKβ, can phosphorylate substrates outside of the known NF-κB inflammatory cascade. Additionally, two other closely related kinases, IKKε and TBK1, share kinase homology with IKKα and IKKβ, but phosphorylate substrates related to IFN regulatory factor (IRF) activation. Despite their well-known roles in NF-κB and IRF activation, we and others have found substrates outside of these signaling cascades. Given this, we have devised a proteomic and bioinformatic approach to identify novel IKK substrates. In the present work, we show IKK-mediated phosphorylation of ITCH, an E3 ubiquitin ligase implicated in the maintenance of mucosal immunologic homeostasis. We identify the site of phosphorylation, and demonstrate the inactivating effect of IKK phosphorylation on ubiquitin ligase activity. Given that mice null for ITCH develop pulmonary interstitial fibrosis and gastritis and given that TNF strongly activates the IKKs and this phosphorylation event, we bred ITCH-/- mice with TNFR1-/- mice to determine if loss of TNF activation of IKKα/β could reverse this phenotype. Both mortality and lung inflammation were improved in TNFR1-/-ITCH-/- when compared with ITCH-/- mice. These results show that bioinformatic and proteomic studies can be coupled with mucosal immunology for novel insights.

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Carreno, Beatriz M., Joel R. Garbow, Grant R. Kolar, Erin N. Jackson, John A. Engelbach, Michelle Becker-Hapak, Leonidas N. Carayannopoulos, David Piwnica-Worms, and Gerald P. Linette. "IMMUNE-DEFICIENT MOUSE STRAINS DISPLAY MARKED VARIABILITY IN GROWTH OF HUMAN MELANOMA LUNG METASTASES (88.6)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 88.6. http://dx.doi.org/10.4049/jimmunol.182.supp.88.6.

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Abstract Immune-deficient mice are widely used in cancer research to study human cancer biology and evaluate new therapeutics. No comprehensive study has been published documenting differences in human tumor engraftment among immune-deficient strains. Using RhoC-expressing human (A375) melanoma cells, we evaluate scid, NOD-scid (NS), NOD-scid β2mnull (NSB), and NOD-scid IL2Rγnull (NSG) as xenograft tumor recipients. Bioluminescence, magnetic resonance imaging and histopathology were employed to monitor serial tumor growth. Melanoma metastases growth is delayed and variable in scid, and NS mice. In contrast, NSB and NSG mice show rapid tumor engraftment, although tumor growth is variable in NSB mice. NK cells were detected in all strains except NSG, and in vitro activated scid, NS and NSB NK cells kill human melanoma lines and primary melanoma cells. Expression of human NKG2D ligands, MICA and MICB, renders melanoma susceptible to murine NK cell-mediated cytotoxicity and killing is inhibited by antibody blockade of murine NKG2D. Murine NKG2D recognition of MICA/B is an important receptor-ligand interaction employed by NK cells in immune-deficient strains to limit engraftment of human tumors. The absolute NK deficiency in NOD-scid IL2Rγnull animals makes this strain an excellent recipient of melanoma and potentially other human malignancies.

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15

Steinmetz, Michael. "Immunology: Immune response restored by gene therapy in mice." Nature 316, no. 6023 (July 1985): 14–15. http://dx.doi.org/10.1038/316014a0.

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LE GOFF, L., C. MARTIN, I. P. OSWALD, P. N. VUONG, G. PETIT, M. N. UNGEHEUER, and O. BAIN. "Parasitology and immunology of mice vaccinated with irradiated Litomosoides sigmodontis larvae." Parasitology 120, no. 3 (March 2000): 271–80. http://dx.doi.org/10.1017/s0031182099005533.

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This study was performed with Litomosoides sigmodontis, the only filarial species which can develop from the infective larvae to the patent phase in immunocompetent laboratory BALB/c mice. Parasitological features and immune responses were analysed up to 3 months before and after challenge inoculation, by comparing 4 groups of mice: vaccinated challenged, challenged only, vaccinated only, and naive mice. Male larvae were very susceptible to irradiation and only female irradiated larvae survived in vivo. Protection, assessed by a lower recovery rate, was confirmed and was established within the first 2 days of challenge. This early reduction of the recovery rate in vaccinated challenged mice was determined by their immune status prior to the challenge inoculation. This was characterized by high specific IgM and IgG subclass (IgG1, IgG2a and IgG3) levels, high specific IL-5 secretion from spleen cells in vitro and a high density of eosinophils in the subcutaneous connective tissue. Six h after the challenge inoculation, most tissue eosinophils were degranulated in vaccinated challenged mice. Thus, in the protocol of vaccination described, protection appeared mainly to result from the stimulation of a Th2 type response and eosinophils seemed to be the main effectors for the increased killing of infective larvae in vaccinated challenged mice. Two months after challenge inoculation, the percentage of microfilaraemic mice was lower in vaccinated challenged mice as a consequence of this overall reduction in the worm load. In both vaccinated challenged and challenged only groups, the in vitro splenocyte proliferative capacity was reduced in microfilaraemic mice.

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Merino, R., M. Iwamoto, L. Fossati, and S. Izui. "Polyclonal B cell activation arises from different mechanisms in lupus-prone (NZB x NZW)F1 and MRL/MpJ-lpr/lpr mice." Journal of Immunology 151, no. 11 (December 1, 1993): 6509–16. http://dx.doi.org/10.4049/jimmunol.151.11.6509.

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Abstract The polyclonal B cell activation is the earliest and most common immunologic abnormality in lupus-prone mice. However, its cellular mechanism(s) has not been well defined. To determine the contribution of CD4+ T cells in this immunologic abnormality, we have depleted CD4+ T cells in lupus-prone (NZB x NZW)F1 and MRL/MpJ-lpr/lpr mice by treating them with anti-CD4 mAb from birth and determined the development of IgM and IgG polyclonal antibody formation. Our results indicate that first, different mechanisms control the development of IgM polyclonal B cell activation in these two autoimmune mice; in (NZB x NZW)F1 mice, IgM polyclonal B cell activation is likely to be a result of an intrinsic B cell defect, whereas CD4+ T cells seem to be responsible for this immunologic abnormality in MRL/MpJ-lpr/lpr mice. Second, the increased production of IgG antibodies, including the IgG3 subclass, was totally regulated by CD4+ T cells in both autoimmune mice. Because IgG3 antibodies can be highly nephritogenic, independent of their immunologic specificities, which is the result of the antibodies' cryoglobulin activity, the active role of CD4+ T cells in the production of IgG3 antibodies in lupus-prone autoimmune mice further strengthens the implication of CD4+ T cells in murine systemic lupus erythematosus.

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Mikó, Irén, Endre Bráth, István Furka, Judit Kovács, David Kelvin, and Robert Zhong. "Spleen autotransplantation in mice: A novel experimental model for immunology study." Microsurgery 21, no. 4 (2001): 140–42. http://dx.doi.org/10.1002/micr.1026.

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Dhar, Payal, Fahmin Basher, Jinyu Zhang, and Jennifer Wu. "Modulation of signaling preference of NK cells by different forms of NKG2D ligands and its implications." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 130.27. http://dx.doi.org/10.4049/jimmunol.198.supp.130.27.

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Abstract The significance of ligand-induced activation of NK cell activating receptor NKG2D has been well established in controlling tumor growth in various experimental animal models. Amongst different types of NKG2D ligands, MHC I chain related molecule MICA/B is expressed most prevalently in various human cancers. In particular, proteolytically shed form of MICA/B (sMIC) has been shown to suppress the immune system and found to correlate with advanced disease stages in cancer patients. Previous studies in our lab using two humanized bi-transgenic mice, one expressing native ligand (TRAMP/MICB) and the other expressing the shedding-resistant mutant (TRAMP/MICB.A2) revealed opposite roles of these ligands in regulating tumor immunity. MICB expressing mice exhibited increased tumor progression, whereas MICB.A2 expressing mice had tumor free survival. These findings raised the intriguing question of why do these structurally similar forms of MIC have vastly different effects on tumor immunity. To address this question, we investigated the signaling events and functional outcomes in NK cells upon stimulation by the two forms of ligands. In vitro co-culture studies of NK cells with tumor cell lines expressing sMICB and MICB.A2 revealed elevated pro-inflammatory and immunosuppressive cytokine production by NK cells upon stimulation with sMICB. In contrast, NK cells stimulated with MICB.A2 displayed enhanced expression of cytotoxicity mediators and signaling molecules of cytotoxicity pathway. This suggests that signaling through sMICB may polarize the NKG2D signaling pathways with preferential activation of inflammatory cytokine pathways. Our data has uncovered a new potential mechanism whereby sMIC promotes tumor progression.

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Valenzuela, Alicia, Cathleen M. Lutz, Stephen Rockwood, and Michael Sasner. "Mouse models for immunology research available from The Jackson Laboratory Repository." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 124.66. http://dx.doi.org/10.4049/jimmunol.196.supp.124.66.

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Abstract The Jackson Laboratory Repository serves as a centralized facility for the development, distribution and cryopreservation of mouse models of human biology and disease. Hundreds of new strains are added annually to one of the largest collections of characterized mouse strains available. This poster presents our newest strains involving genes associated with adaptive immunity. The Pdcdl (programmed cell death 1 - PD1) knockout (KO) mice allow increased infiltration of inflammatory cells in several disease models. CC10-OVA transgenic mice direct OVA expression to lung epithelium; and a KO/KI mouse expresses tamoxifen-inducible cre under the control of the Cd19 promoter in B lymphocytes. New mouse models with mutations in genes involved in the innate immune response include: Dectin-1 (Clec7a) KO mice, which exhibit increased sensitivity to fungal infection and a dysregulated chemokine response; GM-CSF (Csf2) KO mice with impaired phagocytosis, a lupus-like disorder and glomerulonephritis; mice with a KO in MPYS (Tmem173), a pattern recognition receptor that activates type 1 interferon; Ccr2gfp KI/KO mice used in tracking monocyte chemotaxis; a transgenic mouse model of hyperimmunoglobulin E syndrome that expresses modified Stat3; and a new addition to our extensive collection of interleukin mutants, Il1a, a new conditional KO/reporter allele that is produced by monocytes and macrophages. Additionally, several Cas9-expressing lines, requiring only a specific single guide RNA to generate single or multiple simultaneous mutations, are available. These lines overcome the burden of packaging size limits. Researchers are encouraged to deposit mice to the Repository: www.jax.org/donate-a-mouse.

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Yang, Lili, Drake J. Smith, Levina J. Lin, Heesung Moon, Alexander T. Pham, Xi Wang, Siyuan Liu, et al. "Propagating Humanized BLT Mice for the Study of Human Immunology and Immunotherapy." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 157.9. http://dx.doi.org/10.4049/jimmunol.198.supp.157.9.

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Abstract The humanized BLT (bone marrow-liver-thymus) mouse model harbors a nearly complete human immune system, therefore providing a powerful tool to study human immunology and immunotherapy. However, its application is greatly limited by the restricted supply of human CD34+ hematopoietic stem cells and fetal thymus tissues that are needed to generate these mice. The restriction is especially significant for the study of human immune systems with special genetic traits, such as certain HLA (human leukocyte antigen) haplotypes or monogene deficiencies. In order to circumvent this critical limitation, we have developed a method to quickly propagate established BLT mice. Through secondary transfer of bone marrow cells and human thymus implants from BLT mice into NSG (NOD/SCID/IL-2Rγ−/−) recipient mice, we were able to expand one primary BLT mouse into a colony of 4–5 proBLT (propagated BLT) mice in 6–8 weeks. These proBLT mice reconstituted human immune cells, including T cells, at levels comparable to that of their primary BLT donor mouse. They also faithfully inherited the human immune cell genetic traits from their donor BLT mouse, such as the HLA-A2 haplotype that is of special interest for studying HLA-A2 restricted human T cell immunotherapies. Moreover, an EGFP reporter gene engineered into the human immune system was stably passed from BLT to proBLT mice, making proBLT mice suitable for studying human immune cell gene therapy. This method provides an opportunity to overcome a critical hurdle to utilizing the BLT humanized mouse model and enables its more widespread use as a valuable pre-clinical research tool.

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Cross, R. J., J. S. Bryson, and T. L. Roszman. "Immunologic disparity in the hypopituitary dwarf mouse." Journal of Immunology 148, no. 5 (March 1, 1992): 1347–52. http://dx.doi.org/10.4049/jimmunol.148.5.1347.

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Abstract The Snell-Bagg hypopituitary dwarf mouse has been shown to be deficient in growth hormone, thyroxine, and prolactin. There are reports indicating that in addition to these neuroendocrine abnormalities, development of immune competence is also severely impaired in these animals. However, other studies indicate that the immunologic potential of these mice does not differ from their heterozygous littermate controls. Our data show that dwarf mice weaned at 21 days of age and killed at that time, or 7 days later, have reduced numbers of cells in both the spleen and thymus and the mitogen responsiveness of these cells is impaired. However, if mice weaned on day 21 are analyzed at 32 days of age or the mice are weaned at day 30 and analyzed 7 days later the ability to respond to mitogenic stimulation does not differ from controls. Further experiments show that dwarf mice weaned at 30 days of age have a normal complement of V-beta TCR as evidenced by immunofluorescence analysis as well as a primary antibody response to SRBC equivalent to that observed in normal littermates. Immunofluorescence analysis of CD4 and CD8 expression on thymocytes obtained from dwarf mice shows a distinct pattern dependent on the time of weaning and time of analysis. Initial analysis of thymocytes from dwarf mice weaned and killed at 21 days of age do not differ from controls. However, cells from dwarf mice weaned on day 21 and killed on day 28 are markedly different with a loss of immature CD4+/CD8+ cells and a corresponding increase in CD4+ and CD8+ mature thymocytes. In contrast, the phenotype of thymocytes obtained from dwarf mice weaned at 30 days of age and killed on day 37 did not differ from normal littermates. Collectively these studies indicate that hypopituitary dwarf mice lag behind their heterozygous littermates with respect to development of immunocompetence but normal immune responsiveness does develop by 32 days of age when the mice are weaned on day 21.

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Bird, Lucy. "Jinxed mice." Nature Reviews Immunology 7, no. 5 (May 2007): 326–27. http://dx.doi.org/10.1038/nri2085.

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Macchiarini, Francesca, Markus G. Manz, A. Karolina Palucka, and Leonard D. Shultz. "Humanized mice." Journal of Experimental Medicine 202, no. 10 (November 21, 2005): 1307–11. http://dx.doi.org/10.1084/jem.20051547.

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Animal models have been instrumental in increasing the understanding of human physiology, particularly immunity. However, these animal models have been limited by practical considerations and genetic diversity. The creation of humanized mice that carry partial or complete human physiological systems may help overcome these obstacles. The National Institute of Allergy and Infectious Diseases convened a workshop on humanized mouse models for immunity in Bethesda, MD, on June 13–14, 2005, during which researchers discussed the benefits and limitations of existing animal models and offered insights into the development of future humanized mouse models.

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Bashyam, Hema. "Jinxed mice." Journal of Experimental Medicine 204, no. 4 (April 9, 2007): 697a. http://dx.doi.org/10.1084/jem.2044iti4.

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Mountz, J. D., T. Zhou, and L. Johnson. "Production of Transgenic Mice and Application to Immunology and Autoimmunity." American Journal of the Medical Sciences 300, no. 5 (November 1990): 322–29. http://dx.doi.org/10.1097/00000441-199011000-00009.

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Schwartz-Cornil, Isabelle, Michel Bonneau, Marc Dalod, and Nicolas Bertho. "IMPACT OF LARGE MAMMALS MODELS IN IMMUNOLOGY." Reproduction, Fertility and Development 24, no. 1 (2012): 287. http://dx.doi.org/10.1071/rdv24n1ab250.

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Immune responses that control tolerance to self, tolerance to conceptus during pregnancy, and defense against cancer and pathogens are governed by dendritic cells (DC), that are key immune cell types that integrate environment signals and direct T and B cell immune responses. Different DC subtypes exist in mice that each trigger a specific type of immune response, such as cytotoxicity, antibody production, and regulatory processes. Interestingly in mice, it is possible to target specific DC subtypes with antigenised antibodies and obtain a desired type of immune response. However this conceptual breakthrough in vaccinology and immune regulation manipulation may only be valid for laboratory mice, as unfortunately often encountered in the process of bench to bed side translation. Furthermore, whether DC subsets knowledge and manipulation can be translated to human and to animal of socio-economical importance is still not known. We adressed this question in pigs and ruminants. The interest of these species over mice are that (1) they are the direct target species for vaccines, (2) they present genetic diversities and live in an open environment, (3) they present physiological similarities with human such as skin for pigs with skin being a main site for vaccination, (4) skin migrated DC and DC subsets can be collected from lymph after surgical catheterisation of lymph ducts in these species, and not in mice. We studied the molecular characterisation profiles of DC subsets from skin in ruminant and swine and evaluated how they compare to mouse and human DC subsets, based on comparative transcriptomic analyses. We assessed whether ruminant and swine DC subsets share functional similarities and differences with the corresponding murine subsets, and whether these properties translate into novel vaccine developements. Overall our work unravel conserved molecular and functional features that allow characterization of dendritic cell subtypes across mammals and possibly across vertebrates. In the past few decades, a tremendous amount of effort has been invested in developing gene and cell therapies for inherited genetic diseases such as Huntington's disease (HD). However, progress in their clinical application has been very limited. One of the major barriers is the lack of appropriate animal models that allow precise prediction patterns in human patients. Most of the animal models used for gene and cell therapy study are primarily focused on safety and toxicity evaluation, while therapeutic efficacy cannot be fully addressed because they do not carry the same human diseases. Although mouse models of human diseases are available and have been widely used for the development of new therapies, mice are not good predictors for humans because of the fundamental differences (genome composition, body size, life span and metabolic mechanism) between humans and rodents. Although monkeys are one of the best models for studying pharmacokinetics and overall impact of treatment, they are primarily used for safety and toxicity evaluation. Even HD monkey models, created by chemical induction or focal gene transfer in the brain, develop similar cellular pathology, therapeutic efficacy and systemic evaluation cannot be determined, which is one of the major barriers in drug and therapeutic development. The development of transgenic HD monkeys has opened the door for a new paradigm of animal modeling for the advancement of novel gene and cell therapy. HD monkeys not only carry the genetic defect that leads to human HD, they also develop clinical features comparable to humans that no other animal model does. While testing in HD monkeys has yet to be achieved until a cohort of well characterized HD monkeys was established, iPS cell lines derived from HD monkeys with a board spectrum of HD pathology and clinical features are a unique in vitro model for studying HD pathogenesis and the development of novel therapeutic approaches. New knowledge and treatments generated from iPS cells can next be translated and applied in HD monkeys from whom the stem cells were derived, thus the goal of personalized medicine can also be evaluated. This work was funded by a grant from NCRR/NIH (R24RR018827).

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Chaouat, G., J. P. Kolb, N. Kiger, M. Stanislawski, and T. G. Wegmann. "Immunologic consequences of vaccination against abortion in mice." Journal of Immunology 134, no. 3 (March 1, 1985): 1594–98. http://dx.doi.org/10.4049/jimmunol.134.3.1594.

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Abstract CBA/J female mice have a high rate of fetal resorption when mated with DBA/2J males. This fetal wastage can be dramatically reduced by immunizing the female with BALB/cJ but not DBA/2J spleen cells. We report here that immunization with BALB/cJ (but not DBA/2J) spleen cells leads to 1) anti-paternal MHC antibody that is predominantly of the IgG1 isotype, and which disappears from the serum during pregnancy; 2) increased active suppression in both the spleen and placenta; and 3) an ability to adoptively transfer the fetal protection and placental suppression with serum from the immunized mice. Congenic absorption studies before adoptive transfer indicate that the active component of the serum is also directed against the paternal MHC haplotype. These results indicate that maternal humoral immunity can lead to increased fetal protection in correlation with local active suppression in the placenta. They also suggest an expansion of the placental immunoabsorbent hypothesis to include the induction of active suppression against maternal cell-mediated immunity.

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Huntington, Nicholas, and James Di Santo. "Recognition of CD47 on human hematopoietic stem cells results in improved human chimerism in xenografts and permits investigation of rare human progenitors in vivo. (P4469)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 52.2. http://dx.doi.org/10.4049/jimmunol.190.supp.52.2.

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Abstract Human immune system (HIS) mice represent an important biotechnology for fundamental human immunology research, disease models and drug development. The NOD mouse strain has been primarily used in the development of HIS mice as they possess several advantageous polymorphisms. NOD, but not Balb/c mice contain a polymorphism in Sirpα (an inhibitory receptor that prevents phagocytosis upon binding CD47) allowing NOD, but not Balb/c Sirpα to recognize human CD47 on engrafted cells. Despite this, Balb/c immunodeficient mice are still permissive to human engraftment and their use in human immune studies becoming more prevalent. To determine the importance of the CD47-Sirpα interactions in human hematopoietic reconstitution, we generated a congenic Balb/c Rag2-/-γC-/- HIS mouse expressing NOD Sirpα. A functional CD47-Sirpα interaction resulted in significantly higher human chimerism, with specific improvements in T cell, NK cell and progenitor reconstitution compared to HIS mice expressing only Balb/c Sirpα. Improved human reconstitution has allowed us to carefully study bone marrow resident human hematopoietic progenitors. We have identified 2 subsets of CD7+CD244.2+CD38+CD45RA+Lin-(CD56-) bone marrow precursors with either high or exclusive restriction to the NK cell lineage. Our results reveals the degree by which phagocytosis restricts xeno-engraftment and demonstrates a novel, highly sensitive xenograft model for human immunology studies.

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Valenzuela, Alicia, Karen Fancher, Stephen Rockwood, and Cathleen Lutz. "Mouse Models for Immunology Research available from The Jackson Laboratory Repository." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 166.34. http://dx.doi.org/10.4049/jimmunol.200.supp.166.34.

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Abstract The mouse continues to provide researchers a means by which to address complicated immunological questions. The emergence of disruptive genetic engineering technologies have proven to be very applicable to the mouse, spawning a new generation of promising preclinical models. To facilitate access to this flourishing resource, The Jackson Laboratory (JAX) Mouse Repository offers one of the largest sets of well-characterized, genetically engineered mutant mice. Hundreds of new strains are added annually to the collection. Our newest strains include conditionally targeted interleukins, often combined with Cre recombinase and/or reporters. The conditional Il33 knock-out/in (KO/KI) carries an EGFP reporter, a KO/KI to the Il5 gene results in Il15-specific expression of tdTomato and humanized cre, a similar KO/KI to the Il22 gene results in tdTomato/cre expression in intestinal lymphoid tissues, and a KI to Il21 results in expression of Verde green (VFP). Another new strain expresses cre and GFP within peripheral CD8+ T cells. MMRRC program mice include a suite of strains expressing and responding to influenza virus hemagglutinin (HA) neo-self antigen for the study of immune regulation, tolerance and autoimmunity. A Pad4 KO, exhibits absent histone deimination in neutrophils and a defective response to acute infection. KOMP mice, also offered via the MMRRC portion of the JAX Mouse Repository, provide a growing number of targeted immunological mutations. Donating a strain to the Repository fulfills NIH’s requirements for sharing mice. Researchers wishing to have mice considered for inclusion in the Repository are encouraged to submit strains: www.jax.org/donate-a-mouse. This work is supported by NIH, HHMI and private foundations.

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Zhang, Hui, Zhaohui Zhu, Samantha Modrak, and Alex Little. "Tissue-resident memory CD4+ T cells play a dominant role in the initiation of antitumor immunity." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 63.01. http://dx.doi.org/10.4049/jimmunol.208.supp.63.01.

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Abstract Tumor immunology has been studied extensively. Tumor immunology-based cancer immunotherapy has become one of the most promising approaches for cancer treatment. However, one of the fundamental aspects of tumor immunology – the initiation of antitumor immunity – is not fully understood. Compared to that of CD8+ T cells, the effect of CD4+ T cells on antitumor immunity has not been fully appreciated. Using a gene knockout (KO) mouse model – these mice are deficient in TCRa repertoire, specifically lacking iNKT and MAIT cells - we found that the deficiency in TCRa repertoire diversity did not affect the antitumor immunity, at least to melanoma and breast cancer. However, after acquiring thymocytes or splenocytes from wild-type mice, these KO mice exhibited greatly enhanced and long-lasting antitumor immunity. This enhanced antitumor immunity depended on CD4+ T cells, especially tissue-resident memory (TRM) CD4+ T cells, but not iNKT or CD8+ T cells. We also present evidence that CD4+ TRM cells initiate antitumor immunity through IFN-g, and the process is dependent on NK cells but not macrophages. The CD4+ TRM/NK axis appears to control tumor formation and development by eliminating tumor cells and modulating the tumor microenvironment. Taken together, our results demonstrated that CD4+ TRM cells play a dominant role in the initiation of antitumor immunity. Supported by Washington State University Start-up funds

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Dhar, Payal, and Jennifer Wu. "Human NKG2D ligand regulation of Natural Killer cell function and its implications in Cancer and Inflammation." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 170.23. http://dx.doi.org/10.4049/jimmunol.200.supp.170.23.

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Abstract NKG2D is an activating lymphocyte receptor which plays an essential role in stimulating immune responses against tumors. The importance of ligand-induced activation of NKG2D in controlling tumor growth has been well established in various animal models. Amongst diverse NKG2D ligands, MHC I chain related molecule MICA/B is expressed most prevalently in human cancers, but absent in rodents. Proteolytically shed-form of MICA/B (sMIC) has been shown to correlate with advanced cancer stages in patients. Previous studies in our lab using two humanized bi-transgenic mice, one expressing native ligand (TRAMP/MICB) and alternatively expressing shedding-resistant mutant (TRAMP/MICB.A2) revealed opposite roles of the two forms of MIC ligand in tumor immunity. Mice with high levels of sMIC exhibited augmented tumor progression, whereas mice expressing MICB.A2 in tumors enjoyed tumor-free survival; raising an intriguing question of why do these similar forms of MIC have different effects on tumor immunity. To address this, we investigated the signaling events and functional outcomes in NK cells upon stimulation by the two forms of ligands. Co-culture studies of NK cells with tumor cells expressing sMICB and MICB.A2 revealed elevated pro-inflammatory cytokine production by NK cells upon stimulation with sMICB. In contrast, NK cells stimulated with MICB.A2 displayed enhanced expression of cytotoxicity mediators and signaling molecules of cytotoxicity pathway. This suggests that sMICB may polarize the NKG2D signaling pathways with preferential activation of inflammatory cytokine pathways. Our data has uncovered a potential mechanism by which sMIC promotes tumor progression and endorses sMIC as a viable target for cancer immunotherapy.

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Mestas, Javier, and Christopher C. W. Hughes. "Of Mice and Not Men: Differences between Mouse and Human Immunology." Journal of Immunology 172, no. 5 (February 20, 2004): 2731–38. http://dx.doi.org/10.4049/jimmunol.172.5.2731.

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Sacks, David, and Nancy Noben-Trauth. "The immunology of susceptibility and resistance to Leishmania major in mice." Nature Reviews Immunology 2, no. 11 (November 2002): 845–58. http://dx.doi.org/10.1038/nri933.

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Murphy, W. J., S. K. Durum, M. R. Anver, and D. L. Longo. "Immunologic and hematologic effects of neuroendocrine hormones. Studies on DW/J dwarf mice." Journal of Immunology 148, no. 12 (June 15, 1992): 3799–805. http://dx.doi.org/10.4049/jimmunol.148.12.3799.

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Abstract DW/J dwarf mice lack acidophilic anterior pituitary cells and are deficient in growth hormone and other neuroendocrine mediators. These mice were examined to determine the effects of these deficiencies on hematopoietic and immune system development. Previous studies have suggested that these mice had immunologic defects primarily involving T cell development. However, we have found that these mice exhibit decreased peripheral blood cell counts affecting all lineages (erythrocytic, leukocytic, and platelets). Examination of lymphoid tissues of dwarf mice indicated that their spleens were hypoplastic. Treatment of these mice with recombinant human growth hormone resulted in a significant improvement of peripheral blood counts and spleen cell number. Analysis of the bone marrow indicated a profound deficiency of B cell progenitors in the dwarf mice. However, in untreated dwarf mice, mature B cells and T cells were observed in the spleens. Although treatment with recombinant human growth hormone could correct the hematopoietic deficiencies in these mice, it did not restore the B cell progenitor populations, suggesting that an absence of growth hormone is not solely responsible for this deficiency. Thus, these mice display significant myeloid and lymphoid deficiencies that have been previously undetected.

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Kang, Sang-Moo, Eun-Ju Ko, Youri Lee, and Ki-Hye Kim. "Immunology of vaccine adjuvants enhancing respiratory viral vaccine efficacy." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 245.24. http://dx.doi.org/10.4049/jimmunol.204.supp.245.24.

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Abstract We investigated the adjuvant effects of MPL (TLR4 agonist) and CpG (TLR9 agonist) on promoting protection after vaccination of C57BL/6 and BALB/c mice with inactivated influenza split virus or human respiratory syncytial virus (RSV) vaccines. Adjuvant effects of combination MPL and CpG (MPL+CpG) on improving protective vaccine efficacy were evident by higher levels of protective humoral and cellular immune responses to vaccination, more effective control of lung viral replication, prevention of weight loss, and inflammatory cytokines and cellular infiltrates in vaccinated mice after virus challenge. Vaccine-enhanced respiratory disease, a well-known phenomenon due to atypical immune priming by RSV vaccination after challenge, could be prevented by MPL + CpG adjuvants in RSV vaccination, shaping toward Th1 and IgG2a isotype immune responses. In contrast, aluminum hydroxide and squalene oil-in-water adjuvants (AddaVax) were not effective in conferring vaccine-induced protection against influenza and RSV in BALB/c mice after vaccination and challenge. Combination of MPL and CpG was found to exhibit distinct effects on modulating inflammatory micro-environment with cytokines, chemokines, and innate infiltrates in vivo within a day as well as stimulating dendritic cells in vitro to secrete IL-12p70 and TNF-α cytokines. In summary, the findings suggest that a combination adjuvant of different TLR agonists exhibits a unique pattern of innate and adaptive immune responses, contributing to protection by inactivated influenza split virus and subunit RSV vaccination.

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Zhou, Jing, Min Huang, Li-Qing Bi, Su-Ming Zhou, Yun-Lin Cheng, Guo-Xian Ding, and Wei-Hao Sun. "Experimental immunology Bacterial lipoprotein tolerance attenuates cardiac dysfunction in septic mice." Central European Journal of Immunology 3 (2012): 209–20. http://dx.doi.org/10.5114/ceji.2012.30796.

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Tempero, Margaret A., Yoshio Haga, Connie Sivinski, Diane Birt, Lynell Klassen, and Geoffrey Thiele. "Immunologic Effects of Levamisole in Mice and Humans." Journal of Immunotherapy 17, no. 1 (January 1995): 47–57. http://dx.doi.org/10.1097/00002371-199501000-00006.

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Wang, Xianmei, Di Tang, Fei Wang, Gaowei Jin, Lifang Wang, Qun Liu, and Jing Liu. "Microneme Protein 6 Is Involved in Invasion and Egress by Neospora caninum." Pathogens 10, no. 2 (February 13, 2021): 201. http://dx.doi.org/10.3390/pathogens10020201.

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Background: Neospora caninum, is the etiological agent of neosporosis, an infection that causes abortions in cattle and nervous system dysfunction in dogs. Invasion and egress are the key steps of the pathogenesis of N. caninum infection. Microneme proteins (MICs) play important roles in the recognition, adhesion, and invasion of host cells in other apicomplexan parasites. However, some MICs and their functions in N. caninum infection have rarely been reported. Methods: The homologous recombination strategy was used to investigate the function of MIC6 in N. caninum infection. Results: ΔNcMIC6 showed a smaller plaque size and weakened capacities of invasion and egress than Nc1. Transcription levels of the egress-related genes CDPK1, PLP1, and AMA1 of ΔNcMIC6 were downregulated. Due to the lack of NcMIC6, virulence of the pathogen in the infected mouse was weakened. The subcellular localization of NcMIC1 and NcMIC4 in ΔNcMIC6, however, did not change. Nevertheless, the transcription levels of MIC1 and MIC4 in ΔNcMIC6 were downregulated, and the expression and secretion of MIC1 and MIC4 in ΔNcMIC6 were reduced compared with that in Nc1. Furthermore, the absence of NcMIC6 weakened the virulence in mice and lower parasite load detected in mice brains. Conclusions: NcMIC6 is involved in host cell invasion and egress in N. caninum and may work synergistically with other MICs to regulate the virulence of the pathogen. These data lay a foundation for further research into the function and application of NcMIC6.

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Shen, Mengdie, Bibi Zhang, Mengyao Wang, Li’na Meng, and Bin Lv. "Mica Can Alleviate TNBS-Induced Colitis in Mice by Reducing Angiotensin II and IL-17A and Increasing Angiotensin-Converting Enzyme 2, Angiotensin 1-7, and IL-10." Mediators of Inflammation 2020 (October 10, 2020): 1–8. http://dx.doi.org/10.1155/2020/3070345.

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Aim. To explore the treatment effect of mica on 2,4,6-trinitrobenzenesulfonic acid solution- (TNBS-) induced colitis in mice. Materials and Methods. Thirty male BALB/C mice were randomly divided into the control group, the TNBS group, and the mica group. Control mice were treated with saline solution. Experimental colitis was induced by TNBS (250 mg/kg/d) in the TNBS group and the mica group. After modeling, the mica group was treated with mica (180 mg/kg/d) for 3 days, while the TNBS group continued the treatment with TNBS. All solutions were injected intrarectally. During treatment, body weight and mice activity were monitored daily. After treatment, the colon tissues of mice were collected; angiotensin II (Ang II), angiotensin-converting enzyme 2 (ACE2), angiotensin 1-7 (Ang (1-7)), IL-17A, and IL-10 expression was analyzed by ELISA and immunohistochemistry. Results. Food intake, activity, and body weight gradually decreased in the TNBS group compared to the control group and the mica group (all P<0.05). Also, black stool adhesion in the anus and thin and bloody stool were observed in the TNBS group, but not in the other two groups. Moreover, the expression of Ang II, ACE2, Ang (1-7), IL-17A, and IL-10 in the TNBS group increased compared to that in the control group. Compared to the TNBS group, ACE2, Ang (1-7), and IL-10 in the mica group increased, while Ang II and IL-17A decreased (all P<0.05). Conclusion. Mica can alleviate TNBS-induced colitis in mice by regulating the inflammation process; it reduces Ang II and IL-17A and increases ACE2, IL-10, and Ang (1-7).

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Wershil, Barry K. "IX. Mast cell-deficient mice and intestinal biology." American Journal of Physiology-Gastrointestinal and Liver Physiology 278, no. 3 (March 1, 2000): G343—G348. http://dx.doi.org/10.1152/ajpgi.2000.278.3.g343.

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Mutant mice that express abnormalities in mast cell development represent a powerful tool for the investigation of multiple aspects of mast cell biology. In addition, the identification of the genes affected by these mutations has not only increased our knowledge about the mast cell but has opened new areas of investigation as to the role of these gene products in gastrointestinal pathology, immunology, and physiology.

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Ohtsuka, Yoshikazu, Keiko Udaka, Yuichiro Yamashiro, Hideo Yagita, and Ko Okumura. "Dystrophin Acts as a Transplantation Rejection Antigen in Dystrophin-Deficient Mice: Implication for Gene Therapy." Journal of Immunology 160, no. 9 (May 1, 1998): 4635–40. http://dx.doi.org/10.4049/jimmunol.160.9.4635.

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Abstract Duchenne muscular dystrophy is a lethal and common X-linked recessive disease caused by a defect in dystrophin. Normal myoblast transplantation and dystrophin gene transfer have been expected to correct the deficiency in the muscles, but their clinical application has been hampered by the limited preservation of dystrophin-positive myofibers. In this study we investigated the mechanism for immunologic rejection of normal C57BL/10 (B10) myoblasts transplanted into dystrophin-deficient mdx mice, an animal model of Duchenne muscular dystrophy. We found that mdx mice develop CTL specific for dystrophin itself, which were CD8 dominant and restricted by H-2Kb. We identified several antigenic peptides derived from dystrophin that bind to H-2Kb and are recognized by the mdx anti-B10 CTL. Immunologic tolerance against dystrophin was successfully induced by i.v. injection of these peptides before B10 myoblast transplantation, which resulted in sustained preservation of dystrophin-expressing myofibers in mdx mice. These results demonstrate that dystrophin is antigenic in dystrophin-deficient mice and that immunologic regimen would be necessary to achieve the persistent expression of introduced dystrophin in the muscles of dystrophin-deficient individuals.

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Lake, Jeffrey, Leah Rae Donahue, Cathy Lutz, Stephan Rockwood, and Michael Sasner. "The Jackson Laboratory repository: model selection for immunology research (82.10)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S111. http://dx.doi.org/10.4049/jimmunol.178.supp.82.10.

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Abstract The mouse continues as one of the most important model organisms. The Jackson Laboratory Repository serves as a centralized facility for developing, rederiving, cryopreserving and distributing mouse models. The Repository contains a large repertoire of mouse strains related to immunology research that have applications in studies of basic immunology, innate immunity, cancer research, autoimmunity, allergic diseases, and infectious diseases. Selecting appropriate mutant mice is often difficult. For example, mice devoid of CD4+ T cells are found in 3 different strains including a Cd4 −/− strain (B6.129S2-Cd4tm1Mak/J), a strain where MHC class II genes were deleted (B6.129-H2dlAb1-Ea/J), or a targeted mutation in the class II transactivator (B6.129S2-C2tatm1Ccum/J). A wide variety of cre-expressing strains, targeted mutants with loxP-flanked genes and tetracycline regulated transactivator-expressing mice are available that require careful selection. Other factors for model selection include mutation characteristics related to mechanism of action, cell types affected, effects of the mutation on breeding and lifespan, and other associated phenotypes. The strain background including breeding performance, MHC haplotype, disease resistance/susceptibilility and known mutations, such as hemolytic complement deficiency found in a subset of inbred strains, could confound results. Supported by NCRR (RR09781, RR11083, RR16049), NIA, HHMI, and donations from several private foundations

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Pulendran, Bali, and Mark M. Davis. "The science and medicine of human immunology." Science 369, no. 6511 (September 24, 2020): eaay4014. http://dx.doi.org/10.1126/science.aay4014.

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Although the development of effective vaccines has saved countless lives from infectious diseases, the basic workings of the human immune system are complex and have required the development of animal models, such as inbred mice, to define mechanisms of immunity. More recently, new strategies and technologies have been developed to directly explore the human immune system with unprecedented precision. We discuss how these approaches are advancing our mechanistic understanding of human immunology and are facilitating the development of vaccines and therapeutics for infection, autoimmune diseases, and cancer.

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Woloschak, G. E., M. Rodriguez, and C. J. Krco. "Characterization of immunologic and neuropathologic abnormalities in wasted mice." Journal of Immunology 138, no. 8 (April 15, 1987): 2493–99. http://dx.doi.org/10.4049/jimmunol.138.8.2493.

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Abstract Mice bearing the autosomal recessive gene "wasted" (wst/wst) have been reported to develop low or absent secretory immune responses, abnormal DNA repair mechanisms, and uncoordinated body movements. We have performed a detailed immunologic and neuropathologic investigation of the disease. Con A and LPS mitogenic responses of splenic lymphocytes as well as total serum Ig levels were equivalent in wst/wst and undiseased control littermates (wst/+ and +/+). Amounts of serum IgM, IgG2a, IgG2b, IgG3, and IgA, however, were reduced in wst/wst animals. FACS analyses of Ig+ and isotype-specific B cell populations revealed similar percentages of Ig+, mu +, gamma +, and alpha + cells in wst/wst and control mice. However, the percentage of "very bright" Ig+ cells as well as "very bright" heavy and light chain-specific B cell subpopulations was increased at least 10-fold in wst/wst B cells as compared with littermate controls. In addition, studies of Ig-specific mRNA accumulation in these animals revealed significant decreases in all isotypes except gamma 3 in spleens of wst/wst mice as compared with littermate controls. Neuropathologic studies in wst/wst mice showed prominent vacuolar degeneration of neurons within anterior horns of the spinal cord and the motor nuclei of the brain stem. No abnormalities were noted in Purkinje cells of the cerebellum nor within myelin sheaths. The abnormalities in the nervous system resembled human motor neuron disease rather than ataxia-telangiectasia as had been reported previously. The immunologic studies suggest that splenic B cells from wst/wst mice have a defect in the ability to "switch" from membrane to secreted Ig. In addition, this mutation provides a mechanism to study regulatory interactions between the immune and nervous systems.

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Shultz, L. D., P. A. Schweitzer, S. W. Christianson, B. Gott, I. B. Schweitzer, B. Tennent, S. McKenna, L. Mobraaten, T. V. Rajan, and D. L. Greiner. "Multiple defects in innate and adaptive immunologic function in NOD/LtSz-scid mice." Journal of Immunology 154, no. 1 (January 1, 1995): 180–91. http://dx.doi.org/10.4049/jimmunol.154.1.180.

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Abstract The scid mutation was backcrossed ten generations onto the NOD/Lt strain background, resulting in an immunodeficient stock (NOD/LtSz-scid/scid) with multiple defects in adaptive as well as nonadaptive immunologic function. NOD/LtSz-scid/scid mice lack functional lymphoid cells and show little or no serum Ig with age. Although NOD/(Lt-)+/+ mice develop T cell-mediated autoimmune, insulin-dependent diabetes mellitus, NOD/LtSz-scid/scid mice are both insulitis- and diabetes-free throughout life. However, because of a high incidence of thymic lymphomas, the mean lifespan of this congenic stock is only 8.5 mo under specific pathogen-free conditions. After i.v. injection of human CEM T-lymphoblastoid cells, splenic engraftment of these cells was fourfold greater in NOD/LtSz-scid/scid mice than in C.B17/Sz-scid/scid mice. Although C.B-17Sz-scid/scid mice exhibit robust NK cell activity, this activity is markedly reduced in both NOD/(Lt-)+/+ and NOD/LtSz-scid/scid mice. Presence of a functionally less mature macrophage population in NOD/LtSz-scid/scid vs C.B-17Sz-scid/scid mice is indicated by persistence in the former of the NOD/Lt strain-specific defect in LPS-stimulated IL-1 secretion by marrow-derived macrophages. Although C.B-17Sz-scid/scid and C57BL/6Sz-scid/scid mice have elevated serum hemolytic complement activity compared with their respective +/+ controls, both NOD/(LtSz-)+/+ and NOD/LtSz-scid/scid mice lack this activity. Age-dependent increases in serum Ig levels (> 1 micrograms/ml) were observed in only 2 of 30 NOD/LtSz-scid/scid mice vs 21 of 29 C.B-17/Sz-scid/scid animals. The multiple defects in innate and adaptive immunity unique to the NOD/LtSz-scid/scid mouse provide an excellent in vivo environment for reconstitution with human hematopoietic cells.

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Amor, Sandra, Paul A. Smith, Bert 't Hart, and David Baker. "Biozzi mice: Of mice and human neurological diseases." Journal of Neuroimmunology 165, no. 1-2 (August 2005): 1–10. http://dx.doi.org/10.1016/j.jneuroim.2005.04.010.

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Valenzuela, Alicia, Karen Fancher, Stephen Rockwood, and Michael Sasner. "Mouse models for immunology research available from the Jackson Laboratory Repository (HUM1P.318)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 52.43. http://dx.doi.org/10.4049/jimmunol.194.supp.52.43.

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Abstract The Jackson Laboratory Repository serves as a centralized facility for the development, distribution and cryopreservation of mouse models of human biology and disease. Hundreds of new strains are added annually to one of the largest collections of characterized mouse strains available. This poster presents our newest knockout (KO) strains involving genes associated with cell-mediated and humoral immunity. Lag3 (lymphocyte activation 3) KO mice allow further characterization of Treg suppressive function. Pvr (CD155)-null mice carry a lacZ reporter and exhibit inefficient IgA/IgE responses in response to challenge. The loxP-flanked Bcl6 mice carry a conditional allele involved in the differentiation of CD4 T cells into follicular Th cells. Two strains provide reporter/KO mutants of genes involved in the complement pathway, C1qa and Cfb. In addition, the hematopoietic cytokine, Il3, joins our extensive collection of interleukin mutants. New research tools include the following: a strain with EGFP and cre expression from the Zbtb16 (PLZF) promoter, in which expression is directed to the NKT cell lineage; a cre knockin (KI) into the Cx3cr1 promoter region for fate-mapping studies of the monocyte/macrophage compartment; and a ROSA26 KI that features a two-color fluorescent Cre reporter (widespread red fluorescence prior to cre exposure and localized green fluorescence following cre exposure). Researchers are encouraged to deposit mice to the Repository: www.jax.org/donate-a-mouse.

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Valenzuela, Alicia, Cathleen Lutz, Stephen Rockwood, Michael Sasner, and Leah Donahue. "Mouse models for immunology research available from the Jackson Laboratory repository. (IRM9P.718)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 128.1. http://dx.doi.org/10.4049/jimmunol.192.supp.128.1.

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Abstract The Jackson Laboratory Repository serves as a centralized facility for the development, rederivation, distribution and cryopreservation of mouse models of human biology and disease. Hundreds of strains are added annually to one of the largest collections of characterized mouse strains available to the biomedical research community. This poster presents new knockout (KO) strains carrying genes associated with T cells and antigen (Ag) presentation. Lcp2 (SLP-76)-null mice lack T cells and γδ-TCR+ cells. Psmb8 (LMP-7) KO mice exhibit impaired Ag presentation and reduced T cells. In Clec9a (DNGR-1) KO/GFP knock-in (KI) mice, cross-priming of CD8+ T cells against dead-cell-associated antigens is altered. Nlrp3-/- (cryopyrin) mice are useful for studying role of the inflammasome in immune responses. New floxed strains include Cxcl12, Csf1r and a floxed-stop ubiquitous Myc-driven human CD2 KI. Cxcl12 functions in lymphoid progenitor and hematopoietic SC maintenance. The cytokine, Csf1r, is associated with macrophage function. Other additions include: a tamoxifen-inducible KI of EGFP/cre/ERT into the Foxp3 locus, a transcription factor required for development and function of Treg cells; a Notch reporter with GFP expression directed to the Notch pathway; an RORgamma-driven cre transgene that directs expression to αβ T cells, immature thymocytes and lymphoid tissue inducer cells. To have your strain considered for inclusion in the Repository please visit www.jax.org/donate-a-mouse.

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Müller, W., K. Rajewsky, and R. Kühn. "Interleukin-4-deficient mice." Research in Immunology 144, no. 8 (January 1993): 637–38. http://dx.doi.org/10.1016/s0923-2494(05)80018-5.

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Journal articles on the topic 'Mice – Immunology'

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