Relevant bibliographies by topics / Mice – Immunology

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Mice – Immunology'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Mice – Immunology.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
10

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Mice – Immunology"

1

Riley, E. M. "The immunology of experimental Echinoccus granulosus infection in mice." Thesis, University of Liverpool, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.332701.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Rottinghaus, Erin Kay. "Pulmonary Innate Immune Mechanisms in Old Mice." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1237473771.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Peugh, W. N. "The genetics and immunology of cardiac allograft rejection in inbred mice." Thesis, University of Oxford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.375315.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Manoukian, Raffi. "The microenvironmental organization of early B cell precursors in the femoral bone marrow of mutant SCID mice, SCOD/myc transgenic mice and alternate fraction x-irradiated endocolonized mice /." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=57003.

Full text
Abstract:
The in situ microenvironmental organization of early precursor B cells in mouse bone marrow has been studied using three experimental models: (1) mutant mice with severe combined immunodeficiency (SCID), which develop pro-B cells but no pre-B and B cells; (2) SCID/myc transgenic mice having expanded pro-B cell populations, but no pre-B and B cells; (3) x-irradiated C3H/HeJ mice during early stages in the regeneration of pro-B cells in bone marrow seeded from a shielded marrow site. The in vivo localization of B220$ sp+$ cells was revealed by the binding of i.v. injected $ sp{125}$I-mAb 14.8 detected by light and electron microscope radioautography of femoral marrow sections. Many B220$ sp+$ pro-B cells were located in peripheral regions of SCID and SCID/myc bone marrow, often in clusters, associated with an electron dense extracellular matrix and with the processes of stromal reticular cells. Many B220$ sp+$ cells were associated with macrophages which contained numerous ingested bodies. Macrophage associations were more numerous in SCID/myc than in SCID mice, especially in the peripheral marrow regions. 3-5 day post-irradiation endocolonizing marrow contained increasing numbers of B220$ sp+$ cells in subosteal and peripheral regions, situated both within sinusoids and extravascularly, associated with stromal reticular cell processes and often close to nerve fibers. The results demonstrate that early B220$ sp+$ precursors begin to differentiate in peripheral marrow regions and develop intimate associations with reticular cells and macrophages. These findings suggest that through these associations, the bone marrow reticular cells promote the early development of the B cell lineage, while the bone marrow macrophages play a role in the elimination of aberrant precursor B cells.
APA, Harvard, Vancouver, ISO, and other styles
5

Huang, Dennis Shihchang. "Immunological changes in retrovirus-infected mice." Diss., The University of Arizona, 1993. http://hdl.handle.net/10150/186463.

Full text
Abstract:
Acquired Immune Deficiency Syndrome (AIDS), a progressive immunodeficiency induced by Human Immunodeficiency Virus (HIV), frequently sets the stage for life-threatening tumors and opportunistic infections. The proposed study focuses on the immunological changes associated with HIV infection. Often superimposed diarrhea, causing malabsorption and malnutrition, leads to further immunosuppression and accelerated deterioration in many patients. The pathomechanism of Cryptosporidium-induced diarrhea is poorly understood and its relation to AIDS urgently requires investigation. We used LP-BM5 murine leukemia virus (MuLV)-infected C57BL/6 mice to model AIDS and thereby study the immunological changes in human retrovirus infection. Production of Th1 cytokines (IL-2 and IFN-γ) was suppressed, whereas Th2 cytokine production (IL-4, IL-5, IL-6, and IL-10) was enhanced in spleen and mesenteric lymph nodes (MLN) during retrovirus infection. However, increased secretion of IFN-γ in the MLN of retrovirus-infected mice may represent incremental production and release by non-Th1 cells. Lymphoid cell population changes in gut-associated lymphoid tissues (GALT) were documented 4 months after retrovirus infection. Total lymphoid cell numbers decreased in Peyer's patches and CD4⁺ cell numbers decreased in the intestinal lamina propria (ILP). Total lymphoid cell numbers increased in MLN but the relative percentages of surface IgA⁺, cytoplasmic IgA⁺ (cIgA⁺), and cIgM⁺ cells were decreased. Cryptosporidium infestation in retrovirus-infected mice decreased following the administration of pooled bovine colostrum containing a high titer of antibody demonstrating the potential efficacy of passive humoral immunity. Changes in the host cellular immune apparatus, following Cryptosporidium infection, were as follows: (1) increased γδ-TCR⁺ cells in the ILP 6 and 10 days post-infection, (2) decreased CD4⁺ cells in the ILP and intraepithelium 10 days post-infection, (3) reduced IgA⁺ and IgG⁺ cells in the ILP 6 and 10 days post-infection, and (4) increased IgE⁺ cells 6 days post-infection. This altered cellular profile indicates the potential for aberrant cytokine production which may be responsible for the compounded immunodeficiency during retrovirus infection. Overall, the findings underscore the importance of understanding both humoral and cell-mediated immunological influences before the rational development of a therapy against opportunistic cryptosporidial infection in AIDS patients can be undertaken.
APA, Harvard, Vancouver, ISO, and other styles
6

Andrén, Maria. "The Role of Fc Gamma Receptors in Experimental Arthritis." Doctoral thesis, Uppsala University, Department of Genetics and Pathology, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4724.

Full text
Abstract:

Induction of collagen-induced arthritis (CIA), an animal model for human rheumatoid arthritis, is dependent on anti-collagen type II (CII) antibodies. The effector mechanism by which autoantibodies contribute to inflammatory reactions in autoimmune diseases is not well understood. In this thesis I have studied the effector pathways used by IgG anti-CII antibodies to initiate arthritis, namely the IgG Fc receptors (FcγRs) and the complement system. We have found that FcγRIII is crucial for development of CIA, as CII-immunized mice lacking this receptor do not develop arthritis and IgG1 and IgG2b anti-CII antibodies require FcγRIII to trigger arthritis when transferred to naïve mice. The antibody-mediated arthritis was further enhanced in mice deficient in the inhibitory FcγRIIB, indicating that FcγRIIB regulates the activation of FcγRIII. Furthermore, we demonstrate that FcγRIII exist as three distinct haplotypes in mice, FcγRIII:H, FcγRIII:V and FcγRIII:T. Mice expressing the FcγRIII:H haplotype are more susceptible to CIA than mice expressing the FcγRIII:V haplotype, indicating that certain FcγRIII haplotype predisposes for CIA. We also show that the most likely FcγRIII-expressing effector cell in CIA is the macrophage, since FcγRIII-expressing macrophages exclusively can induce arthritis in FcγRIII-deficient mice challenged for CIA.

The complement system was also investigated in development of CIA. We found that this effector pathway is also necessary for onset of arthritis, as CIA was inhibited by treatment with anti-complement factor 5 (C5) antibodies. C5-deficient mice could neither develop CIA unless provided with C5-containing sera.

Taken together, the work presented in this thesis indicates that FcγRs and the complement system are crucial for the induction of experimental arthritis. These findings are important for understanding the mechanisms behind rheumatoid arthritis and blocking of these effector pathways may in the future be used as treatment of rheumatoid arthritis.

APA, Harvard, Vancouver, ISO, and other styles
7

Mathai, Lalitha. "Studies of proteoglycan induced arthritis in BALBc mice." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61247.

Full text
Abstract:
Studies of proteoglycan-induced arthritis in mice revealed two previously unidentified features: polymorphonuclear leucocytes in knee joint cavities and sacroiliac joint involvement. Immunological studies of cellular responses to the proteoglycan revealed a lack of response prior to arthritis which was produced by a further injection. Further studies revealed that depletion of suppressor/cytotoxic T cells in vitro led to an increased response to antigen. Cellular responses in immune and preimmune mice involve helper T lymphocytes. The preimmune but not immune responses wee inhibited by mouse serum and involved a helper T cell dependent response. It did not involve detectable cell death or suppressor/cytotoxic T lymphocytes. Bacteria isolated from mice did not produce arthritis and showed no immune cross-reactivity with proteoglycan.
APA, Harvard, Vancouver, ISO, and other styles
8

Macht, Lisa. "Human autoantibody production in SCID mice." Thesis, University of Bristol, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335368.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Dehlawi, M. S. "Mast cell responses to intestinal nematodes in mice." Thesis, University of Nottingham, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376170.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Madison, Sharon L. "THE EFFECTS OF PM2.5 ON ALLERGIC INFLAMMATION IN MAST CELL DEFICIENT MICE." NCSU, 2002. http://www.lib.ncsu.edu/theses/available/etd-05082002-132938/.

Full text
Abstract:
MADISON, SHARON LYNN. The effects of PM2.5 on allergic inflammation in mast cell deficient mice. (Under the direction of Bruce Hammerberg.) Animal models of asthma have confirmed epidemiological findings that exposure to fine particulate matter (PM2.5) can enhance asthmatic symptoms, including eosinophilic inflammation and airway hyperresponsiveness. Critics have dismissed the possibility that these studies utilizing artificial exposure scenarios, like intratracheal instillation (i.t.), can be legitimately extrapolated to human risk largely due to the fact that the doses required for this type of model exceed the normal ambient concentrations of PM2.5. In order to improve the credibility of the findings from previous animal studies utilizing the i.t. method for delivery of aqueous particle suspensions to the lung, and to determine the biological mechanisms responsible for the observed enhancement of allergic inflammation following PM2.5 exposure, large-scale air samplers have been developed making it possible to directly expose wild type (WT) and genetically altered mice to fine, concentrated ambient particles (CAPs). In this study allergic asthma was modeled in both WT and mast cell deficient (MCD) mice by local (L) or systemic (S) sensitization to ovalbumin (OVA). Two weeks later mice were challenged with OVA (day 0) and then exposed to CAPs (day 0 & 1) with numerous endpoints collected (day 0-2). Overall, there was a temporal difference in the bronchoalveolar lavage cell profile between L and S sensitized mice, and the contribution of mast cells (MC) to this differential response was best observed for neutrophils at day 0 and day 1. Compared to air exposed mice, CAPs depressed total inflammatory cell infiltrates in the bronchoalveolar lavage fluid at day 0 and day 1 after OVA challenge for all groups. This overwhelming difference of limited cellular infiltration of monocytes and neutrophils in the bronchoalveolar lavage fluid following CAPs exposure, and the significant difference between the L and S sensitization protocols, confound interpretation for all of the factors examined. However, the specific finding that CAPs can enhance eosinophil recruitment by day 2 after OVA challenge indicates that the results from previous animal studies utilizing i.t. PM2.5 exposures do in fact support the epidemiological associations linking PM2.5 exposures with the enhancement of allergic inflammation indicative of the asthmatic phenotype. Given the strict regulation of immunological tolerance at mucosal surfaces like the lung, the genetic variability of different mouse strains, and the daily changes in ambient PM2.5 composition, the findings of this study prompt many unique questions. However, the bottom line is that this study demonstrates that ambient PM2.5 does alter Th2-like responses in mice by enhancing pulmonary BAL eosinophils in the late phase response (day 2), and that mast cells are critical to their recruitment.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Mice – Immunology"

1

Immunology of nude mice. Boca Raton, Fla: CRC Press, 1989.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Blanka, Říhová, and Větvička Václav 1954-, eds. Immunological disorders in mice. Boca Raton: CRC Press, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Horst, Bluethmann, and Ohashi Pamela S, eds. Transgenesis and targeted mutagenesis in immunology. San Diego: Academic Press, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

EMBO Workshop (1989 Basel Institute for Immunology). The Scid mouse: Characterization and potential uses :EMBO Workshop held at the Basel Institute for Immunology, Basel, Switzerland, February 20-22, 1989. Berlin: Springer-Verlag, 1989.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

H, Fiebig H., and Berger D. P, eds. Immunodeficient mice in oncology. Basel: Karger, 1992.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Egorov, I. K. Transgenic Mice and Mutants in MHC Research. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Kim, Chŏng-hun. Mausŭ e issŏsŏ sŭkʻuallen i myŏnyŏk panŭng e michʻinŭn yŏnghyang: The effect of squalene on the immune response in ICR mice. Korea: s.n., 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

The use of SCID mice in the investigation of human autoimmune disease. Austin: R.G. Landes, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

1930-, Wu Bing-quan, and Zheng Jie, eds. Immune-deficient animals in experimental medicine. Basel: Karger, 1989.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

International Workshop on Immune-Deficient Animals (6th 1988 Beijing, China). Immune-deficient animals in experimental medicine. Edited by Wu Bing-quan 1930- and Zheng Jie. Basel: Karger, 1989.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Mice – Immunology"

1

Chen, X., Y. Matsuura, and J. F. Kearney. "CD5 Transgenic Mice." In Current Topics in Microbiology and Immunology, 209–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79275-5_25.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Gassel, A. M., and A. Greiner. "Mucosal Immunology of the Small Bowel." In Organtransplantation in Rats and Mice, 417–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72140-3_42.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Phillips, R. A., M. A. S. Jewett, and B. L. Gallie. "Growth of Human Tumors in Immune-Deficient scid Mice and nude Mice." In Current Topics in Microbiology and Immunology, 259–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74974-2_31.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Clark, D. A., D. K. Banwatt, J. Manuel, G. Fulop, and B. A. Croy. "Scid Mice in Reproductive Biology." In Current Topics in Microbiology and Immunology, 227–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74974-2_27.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Faust, E. A., D. J. Rawlings, D. C. Saffran, and O. N. Witte. "Development of btk Transgenic Mice." In Current Topics in Microbiology and Immunology, 363–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79275-5_42.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Woloschak, G. E., M. Rodriguez, and C. J. Krco. "Immunoglobulin Gene Expression in Wasted Mice." In Recent Advances in Mucosal Immunology, 23–30. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5344-7_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Sarvetnick, N., D. Liggitt, and T. A. Stewart. "Inflammatory Destruction of Pancreatic Islets in Interferon Gamma Transgenic Mice." In Progress in Immunology, 821–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83755-5_111.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Cory, S., W. S. Alexandar, H. Rosenbaum, D. L. Vaux, W. Y. Langdon, M. L. Bath, J. McNeall, E. Webb, J. M. Adams, and A. W. Harris. "Transgenic Mice as Models for the Development of Haemopoietic Neoplasia." In Progress in Immunology, 494–501. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83755-5_65.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Figueroa, F., H. Tichy, R. J. Berry, and J. Klein. "MHC Polymorphism in Island Populations of Mice." In The Wild Mouse in Immunology, 100–105. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71304-0_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Haas, Werner, and Ralf Kühn. "Knock out Mice Models for Immunodeficiency Diseases." In Progress in Immunology Vol. VIII, 561–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-51479-1_73.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Mice – Immunology"

1

Confino, Hila, Shay Yarkoni, Matan Goldshtein, Elya Dekel, Omer Lerner, Shani Puyesky, Steve Lisi, et al. "Abstract PO072: Nitric oxide tumor ablation stimulates an anti-tumor immune response in mice." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-po072.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Moslehi, Javid J. "Abstract IA10: Immune checkpoint inhibitor-associated cardiotoxicities: Learning from mice and humans." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-ia10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Fletcher, Jonathan S., Jianqiang Wu, Walter J. Jessen, Jay Pundavela, Eva Dombi, Mi-Ok Kim, Tilat A. Rizvi, Kashish Chetal, Nathan Salomonis, and Nancy Ratner. "Abstract B32: Cxcr3-expressing leukocytes are necessary for neurofibroma formation in mice." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-b32.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Berzofsky, Jay A., Masaki Terabe, and Lauren V. Wood. "Abstract B26: Translation of cancer vaccine strategies from mice to clinical trials." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-b26.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Hackett, Justin, James Glassbrook, Maria Muniz, and Heather M. Gibson. "Abstract P060: Identification of host-intrinsic resistance mechanisms to immune checkpoint inhibitors (ICI) in Diversity Outbred mice." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 5-6, 2021. American Association for Cancer Research, 2022. http://dx.doi.org/10.1158/2326-6074.tumimm21-p060.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Leung, Carol SK. "Abstract A78: Analysis of ROR1 protein expression in mice with reconstituted human immune system components." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-a78.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Chen, Chang-Yu, Satoshi Ueha, Shoji Yokochi, Yoshiro Ishiwata, Haru Ogiwara, Shungo Deshimaru, and Kouji Matsushima. "Abstract B11: Low-dose HMGN1 synergistically enhances antitumor immunity in CD4 depleting antibody-treated mice." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-b11.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Arellano, Danna L., Patricia Juárez, Paloma S. Almeida-Luna, Felipe Olvera, Samanta Jiménez, and Pierrick G. J. Fournier. "Abstract P033: Bone microenvironment-suppressed T cells increase osteoclast formation and the development of osteolytic bone metastases in mice." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 5-6, 2021. American Association for Cancer Research, 2022. http://dx.doi.org/10.1158/2326-6074.tumimm21-p033.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Yao, Li-Chin, Mingshan Cheng, Danying Cai, Leonard D. Shultz, and James G. Keck. "Abstract 3320: Humanized NSG-Tg(Hu-IL15) mice support preclinical immune-oncology efficacy for testing of NK cells based immunology." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-3320.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Cha, Seung, Paul Yazaki, Christine Brown, and John Shively. "Abstract PO083: Treatment of CEA-positive solid tumors with anti-CEA chimeric antigen receptor T-cells in CEA transgenic mice." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 19-20, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/2326-6074.tumimm20-po083.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Mice – Immunology' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography