Journal articles: 'Non-lymphoid cells'

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Dugast, A. S., and B. Vanhove. "Immune regulation by non-lymphoid cells in transplantation." Clinical & Experimental Immunology 156, no. 1 (2009): 25–34. http://dx.doi.org/10.1111/j.1365-2249.2009.03877.x.

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SMINIA, T., A. VANASSELT, M. VDENDE, D. OFHISTOLOGYMEDICAL, and F. FREEUNIVERSITYAMSTERDAMTHEN. "Ontogeny of non-lymphoid cells in rat thymus." Developmental & Comparative Immunology 10, no. 1 (1986): 119. http://dx.doi.org/10.1016/0145-305x(86)90094-7.

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Dijkstra, C. D., and G. Kraal. "Non-lymphoid cells in the splenic white pulp." Research in Immunology 142, no. 4 (1991): 325–28. http://dx.doi.org/10.1016/0923-2494(91)90083-u.

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Huggins, Matthew A., Changwei Peng, Kelsey M. Wanhainen, Abigail R. Gress, Stephen C. Jameson, and Sara E. Hamilton. "Circulating KLRG1+ memory CD8 T cells support immune responses in non-lymphoid tissues." Journal of Immunology 206, no. 1_Supplement (2021): 98.25. http://dx.doi.org/10.4049/jimmunol.206.supp.98.25.

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Abstract The memory T cell population must be durable and capable of responding with rapid effector functions during re-encounter with pathogens. This is accomplished by forming a memory CD8 T cell pool containing multiple distinct subsets of cells that combine varying functional and homing characteristics. At steady-state, memory T cells expressing KLRG1 are restricted to circulation and patrol the host from within the vasculature. These cells convey robust protection during acute rechallenge with pathogens delivered intravenously. Given their localization pattern, we questioned whether KLRG1+ memory T cells participate in immune responses within non-lymphoid tissues. Here, we find that during local and systemically administered infections, KLRG1+ memory cells alter their trafficking pattern and enter infected non-lymphoid tissues. Following intranasal influenza infection, antigen-specific KLRG1+ memory cells proliferate and extravasate into the lung parenchyma. Additionally, during acute LCMV infection, similar findings were observed in all non-lymphoid tissues assayed, including small intestine, kidney, and salivary gland, indicating this is not a unique phenomenon, but rather a consistent trait of these cells. Unexpectedly, progeny from KLRG1+ cells remained within non-lymphoid tissues after acute infection is cleared, downregulating markers of circulation (CX3CR1, KLRG1) and acquiring markers of tissue residency (CD69, CD103). This work challenges the concept that KLRG1+ memory cells are terminally differentiated and demonstrates unappreciated plasticity within this subset to support immunity within non-lymphoid tissues.

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Li, Chaofan, Reshma Taneja, and Jie Sun. "Bhlhe40 maintains CD8+ T cell fitness and functionality in non-lymphoid tissues and tumors." Journal of Immunology 200, no. 1_Supplement (2018): 111.4. http://dx.doi.org/10.4049/jimmunol.200.supp.111.4.

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Abstract Recent evidence has suggested that tissue-resident and tumor-infiltrating CD8 T cells share common molecular signatures for their maintenance in the non-lymphoid environment. Currently, the molecular mechanisms regulating the residency, health and function of effector and memory CD8 T cells in non-lymphoid tissue remain largely elusive. Here we have identified that the transcription factor Bhlhe40 is critical for the fitness and function of effector & memory CD8 T cells in the non-lymphoid tissue and tumor. Bhlhe40 and its associated gene signature are highly expressed in CD8 T cells, which reside in non-lymphoid tissues and tumor, compared with their counterparts in the spleen following viral infection and tumor transplantation. We find that Bhlhe40 deficiency results in the progressive loss of effector and memory CD8 T cells in non-lymphoid tissues following influenza infection and tumor transplantation. As such, Bhlhe40 abolition leads to defective anti-cancer immunity and impaired heterologous anti-viral immunity mediated by the tissue-resident effector and memory CD8 T cells. Mechanistically, we show that Bhlhe40 is dispensable for the activation and metabolic programming of CD8 T cells, but is vital for them maintaining metabolic and mitochondrial fitness. As such, Bhelhe40 deficiency results in energy failure of CD8 T cells and impaired maintenance of active histone marks in the loci of CD8 T cell effector molecules. Therefore, we have identified Bhlhe40 as a key TF for the maintenance of CD8 T cell fitness and functionality in non-lymphoid tissues. Furthermore, our data suggest that the manipulation of Bhlhe40 expression and function may serve as a potential strategy to boost the efficacy of vaccination and immunotherapy.

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Zhenilo, Svetlana, Igor Deyev, Sergey Serov, and Oleg Polanovsky. "Regulation of oct-1 gene transcription is different in lymphoid and non-lymphoid cells." Biochimie 85, no. 7 (2003): 715–18. http://dx.doi.org/10.1016/s0300-9084(03)00121-4.

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Foxwell, Brian M. J., Gaëtane Woerly, Holger Husi, et al. "Identification of several cyclosporine binding proteins in lymphoid and non-lymphoid cells in vivo." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1138, no. 2 (1992): 115–21. http://dx.doi.org/10.1016/0925-4439(92)90050-w.

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ROWISKI, J., P. SICISKI, and J. WARCHO. "Non-random distribution of lymphoid cells within the follicle-associated epithelium is caused by lymphoid cells associated with M cells." Cell Biology International Reports 9, no. 2 (1985): 115. http://dx.doi.org/10.1016/0309-1651(85)90084-0.

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Chen, Zhengshan, Xiaoyan Qiu, and Jiang Gu. "Immunoglobulin Expression in Non-Lymphoid Lineage and Neoplastic Cells." American Journal of Pathology 174, no. 4 (2009): 1139–48. http://dx.doi.org/10.2353/ajpath.2009.080879.

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Inman, Charlotte F., Tamsin Zangerle Murray, Mick Bailey, and Stephen Cose. "Most B cells in non‐lymphoid tissues are naïve." Immunology & Cell Biology 90, no. 2 (2011): 235–42. http://dx.doi.org/10.1038/icb.2011.35.

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van den Oord, J. J., R. De Vos, F. Facchetti, C. De Wolf-Peeters, and V. J. Desmet. "Identification of non-lymphoid cells in inflammatory liver disease." Biochimica et Biophysica Acta (BBA) - Bioenergetics 971, no. 1 (1988): S190. http://dx.doi.org/10.1016/s0005-2728(88)80018-5.

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Peng, Changwei, Matthew A. Huggins, Kelsey M. Wanhainen, et al. "Engagement of ICOS in tissues promotes establishment of CD8+ tissue-resident memory T cells." Journal of Immunology 206, no. 1_Supplement (2021): 24.06. http://dx.doi.org/10.4049/jimmunol.206.supp.24.06.

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Abstract Resident memory T cells (TRM) provide localized protective immunity in non-lymphoid tissues, but the signals and interactions within non-lymphoid tissues involved in generating TRM are incompletely defined. Inducible T-cell costimulator (ICOS) is a costimulatory molecule with well elaborated roles in regulating differentiation of CD4+ T cell populations, its function in CD8+ T cells is largely unexplored. With acute infection models, we found that ICOS-deficient CD8+ T cells showed minimal defects in the initial effector expansion and the generation of recirculating memory subsets. However, consistent with its high expression in TRM, ICOS deficiency significantly compromised the establishment of CD8+ TRM cells in diverse non-lymphoid tissues. We further confirmed that rather than pre-programming the TRM fate during initial T cell priming, the interaction between ICOS ligand (ICOSL) and ICOS in the non-lymphoid tissues during CD8+ T cell recruitment is critical for efficient tissue retention and acquisition of tissue residency signatures. ICOS signaling through PI3K pathway is key for TRM generation and ICOS stimulation promotes downregulation of KLF2, a transcription factor that regulates T cell trafficking, in CD8+ T cells after entering non-lymphoid tissues. Altogether, our data illustrate that engagement of ICOS is one of the critical local costimulatory cues that promote the establishment of tissue-resident populations, with potential implication for therapeutic manipulation.

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Payne, C. M., A. Linde, R. Kibler, B. Poulos, L. Glasser, and R. Fiederlein. "Surface features of human natural killer cells and antibody-dependent cytotoxic cells." Journal of Cell Science 77, no. 1 (1985): 27–46. http://dx.doi.org/10.1242/jcs.77.1.27.

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The purpose of the present study was to examine the surface features of purified large granular lymphocytes (LGLs) (natural killer (NK) cells, antibody-dependent cytotoxic lymphoid (ADCL) cells, K-cells, Fc gamma (+) third population (non-T, non-B) lymphoid cells, T gamma cells) by scanning electron microscopy (SEM) and to compare their surface features with granulocytes, monocytes and Fc gamma (-) lymphoid cells that were all fixed for SEM under identical conditions. We have determined that 72–80% of LGLs enriched by rosette formation with sensitized erythrocytes or using Percoll gradients, have a complex microvillous surface (CMS) pattern identical to that of lymphocytes. The LGL fraction appears by SEM to represent a morphologically homogeneous population of cells. Monocytes prepared for SEM under identical conditions had distinct surface folds and granulocytes displayed numerous broad-based ridge-like profiles. The majority of lymphoid cells in an unfractioned population have a CMS pattern when incubated at room temperature (25 degrees C) before fixation, and a sparse microvillous surface (SMS) pattern when incubated at body temperature (37 degrees C). Ficoll-Hypaque (FH) also had a direct effect on the cell surface pattern. Over half of the unfractionated lymphoid cells displayed a CMS pattern after cells were washed free of FH and incubated at 37 degrees C before fixation. The CMS pattern is therefore not unique to LGLs but can be produced by the surface alteration of non-LGLs found in unfractionated buffy coat and mononuclear fractions. The interactions between LGLs and sensitized erythrocytes in an antibody-dependent cytotoxic assay system, and LGLs and K562 target cells in an NK assay system, were also examined. This is the first report that describes the surface features of human LGLs interacting with K562 target cells in an NK assay system. The LGL populations studied by SEM were determined to have a high percentage of Leu-11(+) and Leu-7(+) cells. These same population were also shown to have high antibody-dependent cytotoxicity and NK activity using the 51Cr release assay.

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Lorenzo-Anota, Helen Yarimet, Diana G. Zarate-Triviño, Jorge Alberto Uribe-Echeverría, et al. "Chitosan-Coated Gold Nanoparticles Induce Low Cytotoxicity and Low ROS Production in Primary Leucocytes, Independent of Their Proliferative Status." Pharmaceutics 13, no. 7 (2021): 942. http://dx.doi.org/10.3390/pharmaceutics13070942.

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(1) Background: Chitosan-coated gold nanoparticles (CH-AuNPs) have important theranostic applications in biomedical sciences, including cancer research. However, although cell cytotoxicity has been studied in cancerous cells, little is known about their effect in proliferating primary leukocytes. Here, we assessed the effect of CH-AuNPs and the implication of ROS on non-cancerous endothelial and fibroblast cell lines and in proliferative lymphoid cells. (2) Methods: The Turkevich method was used to synthetize gold nanoparticles. We tested cell viability, cell death, ROS production, and cell cycle in primary lymphoid cells, compared with non-cancer and cancer cell lines. Concanavalin A (ConA) or lipopolysaccharide (LPS) were used to induce proliferation on lymphoid cells. (3) Results: CH-AuNPs presented high cytotoxicity and ROS production against cancer cells compared to non-cancer cells; they also induced a different pattern of ROS production in peripheral blood mononuclear cells (PBMCs). No significant cell-death difference was found in PBMCs, splenic mononuclear cells, and bone marrow cells (BMC) with or without a proliferative stimuli. (4) Conclusions: Taken together, our results highlight the selectivity of CH-AuNPs to cancer cells, discarding a consistent cytotoxicity upon proliferative cells including endothelial, fibroblast, and lymphoid cells, and suggest their application in cancer treatment without affecting immune cells.

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Boss, Valerie, Deepa J. Talpade, and Thomas J. Murphy. "Induction of NFAT-mediated Transcription by G-coupled Receptors in Lymphoid and Non-lymphoid Cells." Journal of Biological Chemistry 271, no. 18 (1996): 10429–32. http://dx.doi.org/10.1074/jbc.271.18.10429.

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Műzes, Györgyi, Bettina Bohusné Barta, and Ferenc Sipos. "Colitis and Colorectal Carcinogenesis: The Focus on Isolated Lymphoid Follicles." Biomedicines 10, no. 2 (2022): 226. http://dx.doi.org/10.3390/biomedicines10020226.

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Gut-associated lymphoid tissue is one of the most diverse and complex immune compartments in the human body. The subepithelial compartment of the gut consists of immune cells of innate and adaptive immunity, non-hematopoietic mesenchymal cells, and stem cells of different origins, and is organized into secondary (and even tertiary) lymphoid organs, such as Peyer’s patches, cryptopatches, and isolated lymphoid follicles. The function of isolated lymphoid follicles is multifaceted; they play a role in the development and regeneration of the large intestine and the maintenance of (immune) homeostasis. Isolated lymphoid follicles are also extensively associated with the epithelium and its conventional and non-conventional immune cells; hence, they can also function as a starting point or maintainer of pathological processes such as inflammatory bowel diseases or colorectal carcinogenesis. These relationships can significantly affect both physiological and pathological processes of the intestines. We aim to provide an overview of the latest knowledge of isolated lymphoid follicles in colonic inflammation and colorectal carcinogenesis. Further studies of these lymphoid organs will likely lead to an extended understanding of how immune responses are initiated and controlled within the large intestine, along with the possibility of creating novel mucosal vaccinations and ways to treat inflammatory bowel disease or colorectal cancer.

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Borikar, Sneha, Vivek Philip, Lauren Kuffler, and Jennifer J. Trowbridge. "Lysine Methyltransferase Kmt5a Restricts Myeloid-Biased Output of Lymphoid-Primed Multipotent Progenitors." Blood 128, no. 22 (2016): 1487. http://dx.doi.org/10.1182/blood.v128.22.1487.1487.

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Abstract Distinct, lineage-biased subsets of multipotent progenitor cells (MPP) dynamically respond to the demands of the hematopoietic system to replenish mature hematopoietic cells as needed. It currently remains unclear as to whether distinct epigenetic mechanisms regulate lineage-specific expansion and differentiation from MPPs. Focusing on lymphoid-primed multipotent progenitor cells (LMPP/MPP4), we performed a lentiviral shRNA screen of 15 epigenetic factors, selected based on differential expression between myeloid-restricted and lymphoid-restricted progenitors. Following a 48 hour infection with lentiviral shRNA constructs or a non-targeting control, the lineage potential of lymphoid-primed multipotent progenitors was interrogated by myeloid and lymphoid colony forming unit (CFU) assays. From this screen, knockdown of the lysine methyltransferase Kmt5a most dramatically altered lineage output from lymphoid-primed multipotent progenitors through an expansion of myeloid lineage colonies without altering lymphoid colony production. To confirm target specificity, two independent shRNA hairpins targeting distinct locations of the Kmt5a transcript demonstrated that knockdown of Kmt5a (97.1% and 99.5% versus non-targeting control shRNA) increased macrophage colony production by 1.94 and 1.95 fold, respectively (P < 0.01 and P < 0.05, n = 3). Preliminary single cell culture experiments support that the enhanced myeloid lineage output from lymphoid-primed multipotent progenitors occurs at the single-cell level through increased cloning efficiency of myeloid-biased cells. Our results suggest that Kmt5a functions to restrict myeloid lineage output from lymphoid-primed multipotent progenitors. Mechanistically, KMT5A is responsible for monomethylation of histone H4K20 and the methylation of non-histone proteins (ex. p53K376). Our ongoing work aims to distinguish between these histone and non-histone targets to determine the precise mechanisms restricting myeloid lineage output from lymphoid-primed multipotent progenitors. This work has direct implications for a better understanding of the molecular drivers of transient myeloid lineage reprogramming of lymphoid-primed multipotent progenitors during hematopoietic regeneration, age associated myeloid lineage skewing of hematopoiesis, and myeloid malignancies. Disclosures No relevant conflicts of interest to declare.

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Niedobitek, G., H. Herbst, LS Young, et al. "Patterns of Epstein-Barr virus infection in non-neoplastic lymphoid tissue." Blood 79, no. 10 (1992): 2520–26. http://dx.doi.org/10.1182/blood.v79.10.2520.2520.

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Abstract Taking advantage of the abundant expression of the small Epstein-Barr virus (EBV)-encoded RNAs (EBERs) in latently infected cells, we have analyzed 72 normal and hyperplastic lymph nodes and three tonsils of acute infectious mononucleosis (IM) for the presence and distribution of EBV+ cells using EBER-specific in situ hybridization, in some cases combined with immunohistologic demonstration of cell type- characteristic antigens. In IM, large numbers of EBV+ lymphoid B blasts were detectable in extrafollicular areas, whereas germinal centers were generally free of EBV+ cells. In reactive lymph nodes, the frequency of EBV+ cells varied with the degree of lymphoid hyperplasia and underlying immune status. The lowest numbers of EBV+ cells were detected in nonactivated lymph nodes and highest in human immunodeficiency virus-associated lymphadenopathy. If present in these lymph nodes, EBV+ cells were almost exclusively localized to extrafollicular areas, as also observed in IM. However, in contrast to IM, these cells were mainly small lymphocytes. Furthermore, in some instances, occasional scattered EBV+ cells were seen within germinal centers, and in two cases diffuse expansions of EBV+ cells occurred within a single germinal center each, indicating that under certain circumstances EBV+ B lymphocytes may participate in physiologic germinal center reactions. These findings reflect the interference of EBV with physiologic lymphoid differentiation pathways and provide a link to EBV-associated malignant lymphomas with a postulated origin from germinal center cells.

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Niedobitek, G., H. Herbst, LS Young, et al. "Patterns of Epstein-Barr virus infection in non-neoplastic lymphoid tissue." Blood 79, no. 10 (1992): 2520–26. http://dx.doi.org/10.1182/blood.v79.10.2520.bloodjournal79102520.

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Taking advantage of the abundant expression of the small Epstein-Barr virus (EBV)-encoded RNAs (EBERs) in latently infected cells, we have analyzed 72 normal and hyperplastic lymph nodes and three tonsils of acute infectious mononucleosis (IM) for the presence and distribution of EBV+ cells using EBER-specific in situ hybridization, in some cases combined with immunohistologic demonstration of cell type- characteristic antigens. In IM, large numbers of EBV+ lymphoid B blasts were detectable in extrafollicular areas, whereas germinal centers were generally free of EBV+ cells. In reactive lymph nodes, the frequency of EBV+ cells varied with the degree of lymphoid hyperplasia and underlying immune status. The lowest numbers of EBV+ cells were detected in nonactivated lymph nodes and highest in human immunodeficiency virus-associated lymphadenopathy. If present in these lymph nodes, EBV+ cells were almost exclusively localized to extrafollicular areas, as also observed in IM. However, in contrast to IM, these cells were mainly small lymphocytes. Furthermore, in some instances, occasional scattered EBV+ cells were seen within germinal centers, and in two cases diffuse expansions of EBV+ cells occurred within a single germinal center each, indicating that under certain circumstances EBV+ B lymphocytes may participate in physiologic germinal center reactions. These findings reflect the interference of EBV with physiologic lymphoid differentiation pathways and provide a link to EBV-associated malignant lymphomas with a postulated origin from germinal center cells.

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Matsuura, Y., T. Matsuoka, and Y. Fuse. "Ultrastructural and immunohistochemical studies on the ontogenic development of bronchus-associated lymphoid tissue (BALT) in the rat: special reference to follicular dendritic cells." European Respiratory Journal 5, no. 7 (1992): 824–28. http://dx.doi.org/10.1183/09031936.93.05070824.

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The ontogenic development of lymphoid and non-lymphoid cells in bronchus-associated lymphoid tissue (BALT) of the rat was studied ultrastructurally and immunohistochemically. In the late foetal period, only the alveolar macrophages showed a weak positivity for leucocyte common antigen, but no immune region associated (Ia) antigen was detected by monoclonal antibody, MAS 043. Mast cells were present. At 6 days of age, Ia-positive cells were observed in the alveolar wall and peribronchial interstitial tissue, and ultrastructurally there was an aggregation of the fibroblastoid mesenchymal cells. By 10 days of age, the aggregation of lymphoid cells together with S-100-positive reticulum cells had formed a BALT-like periarterial lymphoid sheath. In the adult animals, an obvious B-cell area was present in the central part and subepithelium of BALT, whilst in this area, S-100-positive, strongly Ia-positive cells with a dendritic form were observed. These dendritic cells appeared to be identical to the follicular dendritic cells (FDC) seen in the secondary follicles of lymphoid organs. Those cells may be derived from the fibroblastic reticulum cells, and may function to present antigen to lymphocytes.

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Smith, Corinne, Holly Turula, and Christopher Snyder. "Systemic hematogenous maintenance of memory inflation by MCMV infection (VIR4P.1013)." Journal of Immunology 192, no. 1_Supplement (2014): 143.8. http://dx.doi.org/10.4049/jimmunol.192.supp.143.8.

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Abstract Cytomegalovirus (CMV) is a β-herpesvirus that establishes a latent infection and supports the life-long maintenance of very large numbers of virus-specific effector T cells. These T cells remain functional and are found in many organs in the body. Current models propose that, to sustain these populations, reservoirs of viral antigen and/or latently infected cells in lymph nodes stimulate T cell proliferation and differentiation, followed by migration of progeny to non-lymphoid tissues. We tested this model using murine CMV (MCMV). While MCMV transcriptional activity during latency was below our limit of detection, proliferation of MCMV-specific effector T cells was antigen-dependent and was used as a read-out for antigen encounter. As shown previously, T cells within draining lymph nodes divided at a higher rate than cells elsewhere. However, pulse-chase experiments with BrdU failed to reveal migration of recently divided T cells from lymphoid to non-lymphoid tissues. In fact, inflationary cells observed in non-lymphoid organs were primarily perfusion-resistant cells residing in the vasculature. Strikingly, inhibition of T cell egress from lymph nodes did not eliminate T cell division in circulation, and did not prevent the maintenance of the circulating inflationary population during long-term treatment. Together these results suggest that memory inflation in response to MCMV is driven by viral antigen presented by cells that are accessible to the blood supply.

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Pawelec, G., H. ff S. Davies, J. D. Pearson, C. Steele, and G. Brons. "Stimulation of Lymphocyte Proliferation by Non-Lymphoid Porcine Tissue Cells." Tissue Antigens 14, no. 5 (2008): 367–78. http://dx.doi.org/10.1111/j.1399-0039.1979.tb00865.x.

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PENDINO, KIMBERLY J., K. P. CHEPENIK, and R. R. SCHMIDT. "Differential eicosanoid synthesis by murine fetal thymic non-lymphoid cells." Immunology and Cell Biology 70, no. 4 (1992): 237–52. http://dx.doi.org/10.1038/icb.1992.31.

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Jeurissen, Suzan H. M., E. Marga Janse, Guus Koch, and Gerben F. De Boer. "6.9 Distribution and function of non-lymphoid cells in chickens." Developmental & Comparative Immunology 13, no. 4 (1989): 413. http://dx.doi.org/10.1016/0145-305x(89)90136-5.

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van den Oord, Joost J., Rita de Vos, Fabio Facchetti, Jan Delabie, Chris De Wolf-Peeters, and Valeer J. Desmet. "Distribution of non-lymphoid, inflammatory cells in chronic HBV infection." Journal of Pathology 160, no. 3 (1990): 223–30. http://dx.doi.org/10.1002/path.1711600308.

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Anubha, Bajaj. "The Sentient Propagation-Reactive B Cell-Rich Lymphoid Proliferation." Annals of Cytology and Pathology 9, no. 1 (2024): 020–24. http://dx.doi.org/10.17352/acp.000032.

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Reactive B cell-rich lymphoid proliferation is a heterogeneous group of non-neoplastic lymphoid cell proliferation recapitulating diverse B cell lymphomas. The lesion is commonly categorized as nodal and extra-nodal follicular proliferations, nodal and extra-nodal nodular proliferations or nodal and extra-nodal immunoblastic proliferations. Florid follicular hyperplasia is comprised of quantifiably enhanced, disseminated primary and secondary lymphoid follicles with irregular outlines. Hyperplastic Germinal Centres (GCs) are comprised of admixed centroblasts and centrocytes, reactive T cells, Follicular Dendritic Cells (FDCs) and tingible body macrophages. Lymph node architecture depicts lymphoid follicles comprised of cells expressing B cell antigens wherein primary follicles are pre-eminently constituted of small lymphocytes BCL2+, BCL6- and CD10- immune reactivity. Progressive Transformation of Germinal Centre (PTGC) is constituted of singular or few enlarged lymphoid follicles of 4x to 5x magnitude wherein mantle zone cells display extensive invagination into adjacent germinal centres. Hyaline Vascular Castleman’s Disease (HVCD) delineates innumerable lymphoid follicles confined to the lymph node cortex and medulla or diverse extramedullary sites.

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Caucheteux, Stephan M., Souheil A. Younes, and William E. Paul. "CD45RB expression refines delineation of memory CD4 T cells and aids in understanding their development (91.8)." Journal of Immunology 178, no. 1_Supplement (2007): S161. http://dx.doi.org/10.4049/jimmunol.178.supp.91.8.

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Abstract Upon immunization, CD4 T cell stimulation leads to the development of effectors cells and of 2 major subsets of memory cells: central and effector memory cells, the latter often defined by their differential expression of CD62L and CD44. It is still unclear whether central memory cells derive from effectors or are directly induced. Our results have shown that CD44hi cells can be divided into 2 different subtypes depending on their expression level of CD45RB, providing a precise distinction among central and effector memory CD4 T cells. Using these markers, we show that while central memory CD4 T cells are absent in young mice, they are enriched in old and thymectomized animals To understand the properties of the subsets defined by CD45RB and the establishment of the central and effector memory pools, we followed the fate of transferred naïve 5C.C7 T cell receptor transgenic cells, specific for pigeon cytochrome. During the first days following immunization, virtually all the transferred cells adopt the phenotype associated with effector or effector memory cells. After a month, essentially all 5C.C7 cells in lymphoid organs express phenotypes associated with central memory cells, while in the lung effector T cells are still found. Analysis of the mean “life” of these memory cells and their cycling within the lymphoid and the non-lymphoid organs is under investigation. Taken together, these observations suggest that CD45RB, together with CD44 and CD62L, provides a powerful tool to identify and quantitate naïve, effector and memory cells in lymphoid and non-lymphoid organs. This work was supported by the Intramural Research Program of the NIAID.

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Klein, S. C., S. H. van der Burg, L. H. Boer, et al. "Targeting of cytotoxic T cells against leukemic B cells by bispecific antibody (aCD3 x aCD19) does not distract the T cell from its primary target." Journal of Immunology 159, no. 11 (1997): 5545–49. http://dx.doi.org/10.4049/jimmunol.159.11.5545.

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Abstract Bispecific Abs (BsAb) represent a novel format of immunotherapy, recognizing immune effector cells (e.g., T cells), on the one hand, and target cells (e.g., tumor cells), on the other hand. To be successful, cross-linking of the two cell types is necessary for effector cell activation and subsequent killing of the malignant target cells. We asked the question, whether CTL that were incubated with the BsAb aCD3 x aCD19 and malignant B cells and activated to kill the malignant B cells were still able to eliminate their natural target cells (e.g., virus-infected autologous body cells). To test this, HLA-A*0201-restricted, influenza-specific CTL were incubated with BsAb- and HLA-A*0201-positive B lymphoid tumor cells in combination with HLA-A*0201-positive, virus-infected non-B lymphoid cells as natural target cells. The results showed that even in the presence of BsAb and high amounts of tumor B cells, CTL were still capable of eliminating the virus-infected non-B lymphoid target cells; actually, CTL recognized and eliminated the homologous original target cells preferentially.

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IV, Sainova. "Development of Techniques about Production of Recombinant vaccines and cells with Activated Immunogenic potential." Virology & Immunology Journal 4, no. 1 (2020): 1–4. http://dx.doi.org/10.23880/vij-16000232.

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Methods about derivation of myeloid-like and lymphoid-like cells from normal embryonic fibroblasts were developed and tested. Balb/c mice normal mouse embryonic cells from line 3T3 were co-cultivated with mouse malignant myeloma cells, containing inserted. Murine Leukemia Virus (MuLV) (with RNA-genome, Retroviridae family). For this goal, separate subpopulation of normal mouse embryonic fibroblasts were pre-incubated in cultural fluid, supplemented by previous incubation of myeloma cells in it, after subsequent centrifugation and filtration. Other sub-populations of 3T3 cells were co-cultivated with myeloma cells, by addition of cultural fluids plus cellular suspensions of both types. Subsequently, all mixed cultures were freezed after addition of cryo-protector Dimethylsufoxide (DMSO), subsequently thawed and re-incubated in standard laboratory conditions. In the cultures, pre-incubated in cultural fluid, supplemented by previous incubation of mouse malignant myeloma cells, cells in different stages of myeloid/phagocyte and lymphoid/plasmatic cell differentiation were observed, but in addition of suspensions of cells from both types, appearance of hybrid cells of myeloid-like and phagocyte-like, as well as of lymphoid-like and plasmatic cells-like with mouse malignant myeloma cells were noted. The established changes could be explained with the eventual existence of capable to differentiate to various lineages stem-like cellular sub-populations in the general 3T3 cell line. Also, activated fusion between different cells, as well as between cells and viral particles on the influence of DMSO and of the drastic temperature changes was proposed, which could also lead to transfer of nucleotide sequences. On this principle, a possibility for production of recombinant viral vaccines by exchange of nucleotide sequences between cells and viral particles could be suggested. Furthermore, in confirmation of the literature findings, a capability of non-myeloid and non-lymphoid cells to produce membrane receptor glycoproteins was proposed.

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Sowell, Ryan, Magdalena Rogozinska, and Amanda Marzo. "Rapamycin inhibits generation of memory CD8 T cells that localize to mucosal tissues (46.23)." Journal of Immunology 186, no. 1_Supplement (2011): 46.23. http://dx.doi.org/10.4049/jimmunol.186.supp.46.23.

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Abstract A limitation of current vaccine strategies is the inability to generate effective memory CD8 T cell responses in locations relevant to disease transmission. There is a gap in our knowledge of how memory CD8 T cells are generated and maintained in vivo in different tissues. In response to vaccination, CD8 T cells expand, differentiate into effectors and then undergo contraction. The end result is a population of memory CD8 T cells that survive this process. The mammalian target of rapamycin (mTOR) kinase is a critical regulator of many cell processes including proliferation, differentiation, and survival. The drug rapamycin is a selective inhibitor of mTOR and while it is widely used as an immunosuppressant to inhibit allograft rejection, it has also been shown to increase the number of viral memory CD8 T cells found within secondary lymphoid tissues. The factors that account for the discrepancy observed with rapamycin treatment on pathogen-specific versus graft-specific T cells are unclear. Here we demonstrate that despite enhancing generation of memory CD8 T cells in secondary lymphoid tissues, rapamycin inhibits generation of virus-specific memory CD8 T cells found within non-lymphoid tissues such as the lamina propria of the small intestine and vaginal mucosa. Taken together these data suggest that rapamycin treatment results in an increase in functional memory CD8 T cells residing in secondary lymphoid tissues at the expense of memory CD8 T cells in non-lymphoid sites.

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Rothkotter, H. J., T. Kirchhoff, and R. Pabst. "Lymphoid and non-lymphoid cells in the epithelium and lamina propria of intestinal mucosa of pigs." Gut 35, no. 11 (1994): 1582–89. http://dx.doi.org/10.1136/gut.35.11.1582.

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van der Brugge-Gamelkoorn, Gerda J., Marja B. van de Ende, and T. Sminia. "Non-lymphoid cells of bronchus-associated lymphoid tissue of the rat in situ and in suspension." Cell and Tissue Research 239, no. 1 (1985): 177–82. http://dx.doi.org/10.1007/bf00214917.

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Peng, Changwei, and Stephen C. Jameson. "The relationship between CD4+ follicular helper T cells and CD8+ resident memory T cells: sisters or distant cousins?" International Immunology 32, no. 9 (2020): 583–87. http://dx.doi.org/10.1093/intimm/dxaa045.

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Abstract Independent studies over the last decade have characterized the properties of non-circulating CD8+ ‘resident’ memory T cells (TRM), which offer barrier protective immunity in non-lymphoid tissues and CD4+ follicular helper T cells (TFH), which mediate B-cell help in lymphoid sites. Despite their very different biological roles in the immune system, intriguing parallels have been noted between the trafficking properties and differentiation cues of these populations, parallels which have only sharpened with recent findings. In this review, we explore the features that underlie these similarities and discuss whether these indicate meaningful homologies in the development of CD8+ TRM and CD4+ TFH or reflect resemblances which are only ‘skin-deep’.

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Sullivan, Jenna M., Barbara Hoellbacher, and Daniel J. Campbell. "Id3 expression defines anatomically and functionally distinct regulatory T cells." Journal of Immunology 200, no. 1_Supplement (2018): 116.13. http://dx.doi.org/10.4049/jimmunol.200.supp.116.13.

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Abstract The Id (or inhibitor of DNA binding) proteins are small proteins that contain a helix-loop-helix domain and can heterodimerize with E-protein transcription factors. However, the Id proteins lack a DNA binding domain and act as natural dominant negatives of E-protein function. As a powerful transcriptional regulator, Id3 helps control the functional differentiation of CD8+ effector T cells and its expression is essential for regulatory T cell (TR) maintenance and function. Here we show that expression of Id3 is dynamically regulated in TR in a subset- and tissue-specific fashion. Within the TR compartment cTR (CD62LhiCD44lo) uniformly express Id3, however the eTR (CD62LloCD44hi) compartment can be further subdivided into Id3+ and Id3− eTR. Id3− eTR are found in low abundance in lymphoid tissues but are the majority of TR found in non-lymphoid tissue such as the skin and fat. These Id3− eTR express higher levels of inhibitory surface markers and have similar molecular profiles to the recently described ST2+ tissue TR. We propose that Id3 maintains a lymphoid-tissue TR phenotype and loss of Id3 promotes localization and retention of TR in non-lymphoid tissue.

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Kinoshita, Kazuo, Munehiro Uemura, Takahiro Shimizu, Shun Kinoshita, and Hiroyuki Marusawa. "Stepwise generation of AID knock-in and conditional knockout mice from a single gene-targeting event." International Immunology 33, no. 7 (2021): 387–98. http://dx.doi.org/10.1093/intimm/dxab019.

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Abstract Activation-induced cytidine deaminase (AID) encoded by the Aicda gene initiates class-switch recombination and somatic hypermutation of immunoglobulin genes. In addition to this function, AID is also implicated in the epigenetic regulation in pluripotent stem cells and in the oncogenesis of lymphoid and non-lymphoid origins. To examine AID’s role in specific cell types, we developed mouse strains of conditional knockout (Aicda-FL) and knock-in with a red fluorescent protein gene (RFP) inserted into the Aicda locus (Aicda-RFP). These two strains were obtained from a single targeting event in embryonic stem cells by a three-loxP or tri-lox strategy. Partial and complete recombination among the three loxP sites in the Aicda-RFP locus gave rise to Aicda-FL and AID-deficient loci (Aicda-KO), respectively, after mating Aicda-RFP mice with Cre-expressing mice driven by tissue-non-specific alkaline phosphate promoter. We confirmed RFP expression in B cells of germinal centers of intestine-associated lymphoid tissue. Mice homozygous for each allele were obtained and were checked for AID activity by class-switch and hypermutation assays. AID activity was normal for Aicda-FL but partially and completely absent for Aicda-RFP and Aicda-KO, respectively. Aicda-FL and Aicda-RFP mice would be useful for studying AID function in subpopulations of B cells and in non-lymphoid cells.

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Baghdadi, Hamed, Reza Heidari, Mahdi Zavvar, et al. "Long Non-Coding RNA Signatures in Lymphopoiesis and Lymphoid Malignancies." Non-Coding RNA 9, no. 4 (2023): 44. http://dx.doi.org/10.3390/ncrna9040044.

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Lymphoid cells play a critical role in the immune system, which includes three subgroups of T, B, and NK cells. Recognition of the complexity of the human genetics transcriptome in lymphopoiesis has revolutionized our understanding of the regulatory potential of RNA in normal lymphopoiesis and lymphoid malignancies. Long non-coding RNAs (lncRNAs) are a class of RNA molecules greater than 200 nucleotides in length. LncRNAs have recently attracted much attention due to their critical roles in various biological processes, including gene regulation, chromatin organization, and cell cycle control. LncRNAs can also be used for cell differentiation and cell fate, as their expression patterns are often specific to particular cell types or developmental stages. Additionally, lncRNAs have been implicated in lymphoid differentiation, such as regulating T-cell and B-cell development, and their expression has been linked to immune-associated diseases such as leukemia and lymphoma. In addition, lncRNAs have been investigated as potential biomarkers for diagnosis, prognosis, and therapeutic response to disease management. In this review, we provide an overview of the current knowledge about the regulatory role of lncRNAs in physiopathology processes during normal lymphopoiesis and lymphoid leukemia.

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Cooper, Christopher L., Richard R. Hardy, Michael Reth, and Stephen Desiderio. "Non–cell-autonomous hedgehog signaling promotes murine B lymphopoiesis from hematopoietic progenitors." Blood 119, no. 23 (2012): 5438–48. http://dx.doi.org/10.1182/blood-2011-12-397976.

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Abstract The role of hedgehog (Hh) signaling in B lymphopoiesis has remained unclear. We observed that the proliferation of pro-B cells in stromal cocultures was impaired by interruption of Hh signaling, prompting us to investigate whether the target of Hh antagonism was intrinsic or extrinsic to the B-lymphoid compartment. In the present study, using conditional deletion of the pathway activator gene Smo, we found that cell-autonomous Hh signaling is dispensable for B-cell development, B-lymphoid repopulation of the BM, and humoral immune function. In contrast, depletion of the Smo protein from stromal cells was associated with impaired generation of B-lymphoid cells from hematopoietic stem progenitor cells, whereas reciprocal removal of Smo from these cells had no effect on the production of B-cell progenitors. Depletion of Smo from stromal cells was associated with coordinate down-regulation of genes for which expression is associated with osteoblastoid identity and B-lymphopoietic activity. The results of the present study suggest that activity of the Hh pathway within stromal cells promotes B lymphopoiesis in a non–cell-autonomous fashion.

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Zheng, Mingzhu, Kairui Mao, Difeng Fang, et al. "B cell residency but not T cell–independent IgA switching in the gut requires innate lymphoid cells." Proceedings of the National Academy of Sciences 118, no. 27 (2021): e2106754118. http://dx.doi.org/10.1073/pnas.2106754118.

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Immunoglobulin A (IgA)–producing plasma cells derived from conventional B cells in the gut play an important role in maintaining the homeostasis of gut flora. Both T cell–dependent and T cell–independent IgA class switching occurs in the lymphoid structures in the gut, whose formation depends on lymphoid tissue inducers (LTis), a subset of innate lymphoid cells (ILCs). However, our knowledge on the functions of non-LTi helper-like ILCs, the innate counter parts of CD4 T helper cells, in promoting IgA production is still limited. By cell adoptive transfer and utilizing a unique mouse strain, we demonstrated that the generation of IgA-producing plasma cells from B cells in the gut occurred efficiently in the absence of both T cells and helper-like ILCs and without engaging TGF-β signaling. Nevertheless, B cell recruitment and/or retention in the gut required functional NKp46−CCR6+ LTis. Therefore, while CCR6+ LTis contribute to the accumulation of B cells in the gut through inducing lymphoid structure formation, helper-like ILCs are not essential for the T cell–independent generation of IgA-producing plasma cells.

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Fix, A. S., and L. H. Arp. "Conjunctiva-associated Lymphoid Tissue (CALT) in Normal and Bordetella avium-infected Turkeys." Veterinary Pathology 26, no. 3 (1989): 222–30. http://dx.doi.org/10.1177/030098588902600306.

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Conjunctiva-associated lymphoid tissue (CALT) was characterized in normal and Bordetella avium-infected turkey poults during the first 5 weeks of life. At 1, 5, 12, 19, 25, and 33 days post-hatching (DPH), upper and lower eyelids were examined by gross, histologic, and electron microscopic techniques. CALT was confined to the proximal part of the lower eyelid near the conjunctival fornix; it appeared by 5 DPH as individual lymphoid nodules and as dense masses by 19 DPH. In the upper eyelid, CALT was present only as isolated nodules. Histologically. CALT was composed of dense lymphocyte infiltrates within subepithelial connective tissue, intraepithelial lymphocytes, and flattened lymphoid-associated epithelium that lacked goblet cells. Germinal centers were in CALT by 19 DPH. By scanning electron microscopy, epithelial cells over lymphoid areas were flat and had short, irregular microvilli; non-lymphoid areas were covered by cells with tall, regular microvilli. Transmission electron microscopy revealed that with increasing age of birds, the epithelium over conjunctival lymphoid infiltrates became progressively flattened and infiltrated by lymphocytes. Some blood vessels in CALT had high endothelial cells; lymphocytes were in the lumen and between or beneath endothelial cells. In B. avium- infected poults. CALT was increased, developed earlier, and contained more germinal centers than in normal poults. We conclude that CALT of turkeys closely resembles other mucosal lymphoid tissues and may serve as a site for local antigen uptake.

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Carmichael, Catherine L., Donald Metcalf, Katya J. Henley, et al. "Hematopoietic overexpression of the transcription factor Erg induces lymphoid and erythro-megakaryocytic leukemia." Proceedings of the National Academy of Sciences 109, no. 38 (2012): 15437–42. http://dx.doi.org/10.1073/pnas.1213454109.

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The transcription factor encoded by the E-twenty-six (ETS)-related gene, ERG, is an essential regulator of hematopoietic stem cell function and a potent human oncoprotein. Enforced expression of ERG in murine hematopoietic cells leads to the development of a well-characterized lymphoid leukemia and a less well-defined non lymphoid disease. To clarify the latter, we generated murine bone marrow chimeras with enforced Erg expression in engrafted hematopoietic progenitor cells. As expected, these mice developed lymphoid leukemia. However, the previously reported non lymphoid disease that developed was shown to be a uniform, transplantable leukemia with both erythroid and megakaryocytic characteristics. In vivo, this disease had the overall appearance of an erythroleukemia, with an accumulation of immature erythroblasts that infiltrated the bone marrow, spleen, liver, and lung. However, when stimulated in vitro, leukemic cell clones exhibited both erythroid and megakaryocytic differentiation, suggesting that transformation occurred in a bipotential progenitor. Thus, in mice, Erg overexpression induces the development of not only lymphoid leukemia but also erythro-megakaryocytic leukemia.

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Giorno, R. "Immunohistochemical analysis of human peripheral blood and lymphoid tissues using monoclonal antibodies immunoreactive with non-lymphoid cells." Histochemistry 84, no. 3 (1986): 241–45. http://dx.doi.org/10.1007/bf00495789.

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Chuluunbaatar, Tsolmon, Osamu Ichii, Md Abdul Masum, Takashi Namba, and Yasuhiro Kon. "Morphological Characteristics of Genital Organ-Associated Lymphoid Tissue in the Vaginal Vestibule of Goats and Pigs." Veterinary Sciences 10, no. 1 (2023): 51. http://dx.doi.org/10.3390/vetsci10010051.

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Mucosa-associated lymphoid tissue (MALT) is a specialized form of peripheral lymphoid tissue (LT), which is found on mucosal surfaces exposed to the environment. However, morphological data of these tissues in farm animals are scarce. This study investigated the gross anatomical and histological features of genital organ-associated lymphoid tissues (GOALTs) in the vaginal vestibule (VV) of healthy, non-pregnant, adult goats and pigs. Their VVs were composed of stratified squamous, non-keratinized epithelium, and various-sized dark-blue hematoxylin-positive spots were observed in whole-mount specimens, which were diffusely distributed throughout the mucosal surfaces. These spots were histologically identified as LTs and consisted of lymphatic nodules (LNs) or diffuse lymphoid tissue (DLTs). Both LNs and DLTs contained B cells, T cells, macrophages, dendritic cells, plasma cells, and high endothelial venules. Only the numbers of B cells were significantly higher in both the LNs and DLTs of pigs compared to goats. Furthermore, the surface of the VV epithelium covering the LTs was partially disrupted with a large intercellular space containing abundant connective tissue fibers with numerous lymphocytes. In conclusion, GOALTs in the VV appear to be common local immunological barriers in both examined animals. This knowledge is crucial for understanding the structures and disorders of female reproductive organs in farm animals.

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Cairo, Gaetano, Paolo Vezzoni, Lidia Bardella, et al. "Regulation of ferritin synthesis in malignant and non-malignant lymphoid cells." Biochemical and Biophysical Research Communications 139, no. 2 (1986): 652–57. http://dx.doi.org/10.1016/s0006-291x(86)80040-7.

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Klein, Benjamin Y., and Sherie L. Morrison. "Expression of genes containing the IgH enhancer in non-lymphoid cells." Molecular Immunology 27, no. 8 (1990): 713–22. http://dx.doi.org/10.1016/0161-5890(90)90080-j.

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Journal articles on the topic 'Non-lymphoid cells'

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