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  • 1
    Publication Date: 2011-02-12
    Description: Memory B cells formed in response to microbial antigens provide immunity to later infections; however, the inability to detect rare endogenous antigen-specific cells limits current understanding of this process. Using an antigen-based technique to enrich these cells, we found that immunization with a model protein generated B memory cells that expressed isotype-switched immunoglobulins (swIg) or retained IgM. The more numerous IgM(+) cells were longer lived than the swIg(+) cells. However, swIg(+) memory cells dominated the secondary response because of the capacity to become activated in the presence of neutralizing serum immunoglobulin. Thus, we propose that memory relies on swIg(+) cells until they disappear and serum immunoglobulin falls to a low level, in which case memory resides with durable IgM(+) reserves.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993090/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993090/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pape, Kathryn A -- Taylor, Justin J -- Maul, Robert W -- Gearhart, Patricia J -- Jenkins, Marc K -- F32 AI091033/AI/NIAID NIH HHS/ -- R01 AI036914/AI/NIAID NIH HHS/ -- R01 AI039614/AI/NIAID NIH HHS/ -- R37 AI027998/AI/NIAID NIH HHS/ -- T32 CA009138/CA/NCI NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2011 Mar 4;331(6021):1203-7. doi: 10.1126/science.1201730. Epub 2011 Feb 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21310965" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; Antigens, CD38/analysis ; B-Lymphocyte Subsets/*immunology ; Cell Survival ; Female ; Germinal Center/cytology/immunology ; Immunization ; *Immunoglobulin Class Switching ; Immunoglobulin M/genetics/*immunology ; *Immunologic Memory ; Lymph Nodes/cytology/immunology ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Mutation ; Phycocyanin/immunology ; Phycoerythrin/immunology ; Spleen/cytology/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2006-03-04
    Description: Immunity to a plethora of microbes depends on a diverse repertoire of naive lymphocytes and the production of long-lived memory cells. We present evidence here that low clonal abundance in a polyclonal repertoire favors the survival and activation of naive CD4(+) T cells as well as the survival of their memory cell progeny. The inverse relation between clonal frequency and survival suggests that intraclonal competition could help maintain an optimally diverse repertoire of T cells and an optimal environment for the generation of long-lived memory cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hataye, Jason -- Moon, James J -- Khoruts, Alexander -- Reilly, Cavan -- Jenkins, Marc K -- AI27998/AI/NIAID NIH HHS/ -- AI39614/AI/NIAID NIH HHS/ -- F32 AI063793/AI/NIAID NIH HHS/ -- F32 AI063793-01A1/AI/NIAID NIH HHS/ -- T32 CA009138/CA/NCI NIH HHS/ -- T32-AI007313/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 7;312(5770):114-6. Epub 2006 Mar 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA. hata0006@umn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16513943" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; CD4-Positive T-Lymphocytes/*immunology/physiology ; Cell Survival ; Clone Cells/immunology/physiology ; Half-Life ; Histocompatibility Antigens Class II/immunology ; *Immunologic Memory ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Ovalbumin/immunology ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocyte Subsets/*immunology/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2016-01-30
    Description: Infection elicits CD4(+) memory T lymphocytes that participate in protective immunity. Although memory cells are the progeny of naive T cells, it is unclear that all naive cells from a polyclonal repertoire have memory cell potential. Using a single-cell adoptive transfer and spleen biopsy method, we found that in mice, essentially all microbe-specific naive cells produced memory cells during infection. Different clonal memory cell populations had different B cell or macrophage helper compositions that matched effector cell populations generated much earlier in the response. Thus, each microbe-specific naive CD4(+) T cell produces a distinctive ratio of effector cell types early in the immune response that is maintained as some cells in the clonal population become memory cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4776317/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4776317/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tubo, Noah J -- Fife, Brian T -- Pagan, Antonio J -- Kotov, Dmitri I -- Goldberg, Michael F -- Jenkins, Marc K -- F32 AI107995/AI/NIAID NIH HHS/ -- R01 AI039614/AI/NIAID NIH HHS/ -- R01 AI106791/AI/NIAID NIH HHS/ -- T32 HL007062/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):511-4. doi: 10.1126/science.aad0483.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immune Mediated Disease Therapy Group, Genzyme, a Sanofi Company, Framingham, MA 01701, USA. ; Department of Medicine, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA. ; Department of Medicine, MRC Laboratory of Molecular Biology, Cambridge, UK. ; Department of Microbiology and Immunology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA. ; Department of Microbiology and Immunology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA. jenki002@umn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823430" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; B-Lymphocytes/immunology ; Bacterial Toxins/immunology ; CD4-Positive T-Lymphocytes/*immunology/*microbiology ; Clone Cells/immunology ; Heat-Shock Proteins/immunology ; Hemolysin Proteins/immunology ; *Immunologic Memory ; Listeria monocytogenes/*immunology ; Listeriosis/*immunology ; Mice ; Mice, Inbred C57BL ; Receptors, CXCR5/genetics/immunology ; Single-Cell Analysis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2015-02-01
    Description: When exposed to antigens, naive B cells differentiate into different types of effector cells: antibody-producing plasma cells, germinal center cells, or memory cells. Whether an individual naive B cell can produce all of these different cell fates remains unclear. Using a limiting dilution approach, we found that many individual naive B cells produced only one type of effector cell subset, whereas others produced all subsets. The capacity to differentiate into multiple subsets was a characteristic of clonal populations that divided many times and resisted apoptosis, but was independent of isotype switching. Antigen receptor affinity also influenced effector cell differentiation. These findings suggest that diverse effector cell types arise in the primary immune response as a result of heterogeneity in responses by individual naive B cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4412594/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4412594/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Taylor, Justin J -- Pape, Kathryn A -- Steach, Holly R -- Jenkins, Marc K -- P01 AI035296/AI/NIAID NIH HHS/ -- P01AI035296/AI/NIAID NIH HHS/ -- P30 CA077598/CA/NCI NIH HHS/ -- R01 AI027998/AI/NIAID NIH HHS/ -- R01 AI039614/AI/NIAID NIH HHS/ -- R01AI036914/AI/NIAID NIH HHS/ -- R37AI027998/AI/NIAID NIH HHS/ -- T32 CA009138/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2015 Feb 13;347(6223):784-7. doi: 10.1126/science.aaa1342. Epub 2015 Jan 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA. Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98019, USA. jtaylor3@fhcrc.org. ; Department of Microbiology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA. ; Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98019, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25636798" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody-Producing Cells/*immunology ; Antigens/immunology ; Apoptosis/*immunology ; B-Lymphocyte Subsets/*immunology ; B-Lymphocytes/*immunology ; Cell Differentiation ; *Immunity, Humoral ; Immunoglobulin Class Switching ; Mice ; Mice, Inbred C57BL
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2016-04-21
    Description: Our current understanding of immunology was largely defined in laboratory mice, partly because they are inbred and genetically homogeneous, can be genetically manipulated, allow kinetic tissue analyses to be carried out from the onset of disease, and permit the use of tractable disease models. Comparably reductionist experiments are neither technically nor ethically possible in humans. However, there is growing concern that laboratory mice do not reflect relevant aspects of the human immune system, which may account for failures to translate disease treatments from bench to bedside. Laboratory mice live in abnormally hygienic specific pathogen free (SPF) barrier facilities. Here we show that standard laboratory mouse husbandry has profound effects on the immune system and that environmental changes produce mice with immune systems closer to those of adult humans. Laboratory mice--like newborn, but not adult, humans--lack effector-differentiated and mucosally distributed memory T cells. These cell populations were present in free-living barn populations of feral mice and pet store mice with diverse microbial experience, and were induced in laboratory mice after co-housing with pet store mice, suggesting that the environment is involved in the induction of these cells. Altering the living conditions of mice profoundly affected the cellular composition of the innate and adaptive immune systems, resulted in global changes in blood cell gene expression to patterns that more closely reflected the immune signatures of adult humans rather than neonates, altered resistance to infection, and influenced T-cell differentiation in response to a de novo viral infection. These data highlight the effects of environment on the basal immune state and response to infection and suggest that restoring physiological microbial exposure in laboratory mice could provide a relevant tool for modelling immunological events in free-living organisms, including humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4871315/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4871315/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beura, Lalit K -- Hamilton, Sara E -- Bi, Kevin -- Schenkel, Jason M -- Odumade, Oludare A -- Casey, Kerry A -- Thompson, Emily A -- Fraser, Kathryn A -- Rosato, Pamela C -- Filali-Mouhim, Ali -- Sekaly, Rafick P -- Jenkins, Marc K -- Vezys, Vaiva -- Haining, W Nicholas -- Jameson, Stephen C -- Masopust, David -- 1R01AI111671/AI/NIAID NIH HHS/ -- R01 AI075168/AI/NIAID NIH HHS/ -- R01 AI084913/AI/NIAID NIH HHS/ -- R01 AI111671/AI/NIAID NIH HHS/ -- R01 AI116678/AI/NIAID NIH HHS/ -- R01AI075168/AI/NIAID NIH HHS/ -- R01AI084913/AI/NIAID NIH HHS/ -- R01AI116678/AI/NIAID NIH HHS/ -- England -- Nature. 2016 Apr 28;532(7600):512-6. doi: 10.1038/nature17655. Epub 2016 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Immunology, Department of Microbiology and Immunology, University of Minnesota, Minneapolis, Minnesota 55414, USA. ; Center for Immunology, Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota 55414, USA. ; Department of Pediatric Oncology, Dana-Farber Cancer Institute, and Pediatric Hematology and Oncology, Children's Hospital, Boston, Massachusetts 02115, USA. ; Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27096360" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animal Husbandry/*methods ; Animals ; Animals, Laboratory/*immunology ; Animals, Wild/*immunology ; Cell Differentiation ; *Environment ; Environmental Exposure ; Female ; Humans ; Immune System/*immunology ; Immunity/*immunology ; Immunity, Innate/immunology ; Immunologic Memory ; Infant, Newborn ; Male ; Mice ; *Models, Animal ; Phenotype ; Specific Pathogen-Free Organisms ; T-Lymphocytes/cytology/immunology ; Virus Diseases/immunology/virology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 1998-07-04
    Description: Early events in the humoral immune response were visualized in lymph nodes by simultaneous tracking of antigen-specific CD4 T and B cells after immunization. The T cells were initially activated in the T cell areas when the B cells were still randomly dispersed in the B cell-rich follicles. Both populations then migrated to the edges of the follicles and interacted there, resulting in CD154-dependent B cell proliferation and germinal center formation. These results provide visual documentation of cognate T-B cell interactions and localize them to the follicular border.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garside, P -- Ingulli, E -- Merica, R R -- Johnson, J G -- Noelle, R J -- Jenkins, M K -- AI27998/AI/NIAID NIH HHS/ -- AI35296/AI/NIAID NIH HHS/ -- AI39614/AI/NIAID NIH HHS/ -- Wellcome Trust/United Kingdom -- etc. -- New York, N.Y. -- Science. 1998 Jul 3;281(5373):96-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Glasgow, Department of Immunology, Western Infirmary, Glasgow, G11 6NT, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9651253" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; *Antibody Formation ; Antigen Presentation ; B-Lymphocytes/cytology/*immunology ; CD4-Positive T-Lymphocytes/cytology/*immunology ; CD40 Ligand ; Cell Movement ; Dendritic Cells/immunology ; Germinal Center/immunology ; Immunization ; Immunoglobulin M/analysis ; Lymph Nodes/cytology/*immunology ; *Lymphocyte Activation ; Membrane Glycoproteins/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; Plasma Cells/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1988-09-23
    Description: Cyclosporine A (CsA) is an important immunosuppressive drug that is widely used in transplantation medicine. Many of its suppressive effects on T cells appear to be related to the inhibition of T cell receptor (TCR)-mediated activation events. Paradoxically, in certain situations CsA is responsible for the induction of a T cell-mediated autoimmunity. The effects of CsA on T cell development in the thymus were investigated to elucidate the physiologic events underlying this phenomenon. Two major effects were revealed: (i) CsA inhibits the development of mature single positive (CD4+8- or CD4-8+) TCR-alpha beta+ thymocytes without discernibly affecting CD4-8- TCR-gamma delta+ thymocytes and (ii) CsA interferes with the deletion of cells bearing self-reactive TCRs in the population of single positive thymocytes that do develop. This suggests a direct mechanism for CsA-induced autoimmunity and may have implications for the relative contribution of TCR-mediated signaling events in the development of the various T cell lineages.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jenkins, M K -- Schwartz, R H -- Pardoll, D M -- New York, N.Y. -- Science. 1988 Sep 23;241(4873):1655-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3262237" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antigens, Differentiation, T-Lymphocyte/genetics ; Autoimmune Diseases/chemically induced ; Cell Differentiation/drug effects ; Cyclosporins/*pharmacology ; Mice ; Mice, Inbred Strains ; Receptors, Antigen, T-Cell/drug effects/genetics ; T-Lymphocytes/*drug effects/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2014-04-18
    Description: T-helper-17 (TH17) cells have critical roles in mucosal defence and in autoimmune disease pathogenesis. They are most abundant in the small intestine lamina propria, where their presence requires colonization of mice with microbiota. Segmented filamentous bacteria (SFB) are sufficient to induce TH17 cells and to promote TH17-dependent autoimmune disease in animal models. However, the specificity of TH17 cells, the mechanism of their induction by distinct bacteria, and the means by which they foster tissue-specific inflammation remain unknown. Here we show that the T-cell antigen receptor (TCR) repertoire of intestinal TH17 cells in SFB-colonized mice has minimal overlap with that of other intestinal CD4(+) T cells and that most TH17 cells, but not other T cells, recognize antigens encoded by SFB. T cells with antigen receptors specific for SFB-encoded peptides differentiated into RORgammat-expressing TH17 cells, even if SFB-colonized mice also harboured a strong TH1 cell inducer, Listeria monocytogenes, in their intestine. The match of T-cell effector function with antigen specificity is thus determined by the type of bacteria that produce the antigen. These findings have significant implications for understanding how commensal microbiota contribute to organ-specific autoimmunity and for developing novel mucosal vaccines.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4128479/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4128479/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Yi -- Torchinsky, Miriam B -- Gobert, Michael -- Xiong, Huizhong -- Xu, Mo -- Linehan, Jonathan L -- Alonzo, Francis -- Ng, Charles -- Chen, Alessandra -- Lin, Xiyao -- Sczesnak, Andrew -- Liao, Jia-Jun -- Torres, Victor J -- Jenkins, Marc K -- Lafaille, Juan J -- Littman, Dan R -- 5P30CA016087-32/CA/NCI NIH HHS/ -- P30 CA077598/CA/NCI NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- R01 AI039614/AI/NIAID NIH HHS/ -- UL1 TR00038/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Jun 5;510(7503):152-6. doi: 10.1038/nature13279. Epub 2014 Apr 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, New York 10016, USA. ; 1] Department of Microbiology, Center for Immunology, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA [2] Mucosal Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-0485, USA. ; Department of Microbiology, New York University School of Medicine, New York, New York 10016, USA. ; Department of Microbiology, Center for Immunology, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA. ; 1] The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, New York 10016, USA [2] Howard Hughes Medical Institute, New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24739972" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Bacterial/chemistry/*immunology ; Bacterial Vaccines ; Cell Differentiation ; Epitopes, T-Lymphocyte/chemistry/immunology ; Gram-Positive Bacteria/chemistry/*immunology ; Hybridomas/immunology ; Immunity, Mucosal/immunology ; Intestinal Mucosa/cytology/immunology ; Intestine, Small/cytology/immunology ; Intestines/cytology/*immunology ; Listeria monocytogenes/immunology ; Mice ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; Receptors, Antigen, T-Cell/immunology ; *Symbiosis ; Th17 Cells/cytology/*immunology
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Immunogenetics 23 (1986), S. 292-301 
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The mechanisms underlying Ir gene control of CMI were addressed by examining the DTH and Tprlf responses specific for the synthetic polymers GT, GAT, and GA. We show that BALB/c mice (GAT/GA responders, GT nonresponders) primed with GT fail to develop DTH and Tprlf responses specific for GT, GAT, or GA. GAT immunization resulted in DTH responses that could be elicited not only with GAT and GA but also with GT, demonstrating that GT-specific TDH are present in nonresponder mice. GT-specific DTH was transferred with Thy-1+ Lyt-1+2−, H-2 Irestricted, nylon wool nonadherent cells. GA-primed BALB/c mice developed GAT- and GA-, but not GT-apecific DTH responses, indicating that GA and GT do not cross-react at the T-cell level. The ability of GAT [but not a mixture of GA plus GT, or GT electrostatically complexed to the immunogenic carrier MBSA (GT-MBSA)] to induce GT-specific DTH suggested a requirement for covalent linkage of stimulatory ‘GA’ and nonstimulatory ‘GT’ determinants present on the GAT molecule. Similarly, GT-specific in vitro Tprlf responses could be demonstrated in GAT-primed mice exhibiting significant levels of GT-specific DTH but not in GT- or GT-MBSA-primed mice. Tolerization experiments also suggested that GT-specific Th were involved in the development of GT-specific DTH in GAT-primed mice. The GT nonresponsiveness of BALB/c mice for DTH and Tprlf responses could not be reversed by treatments designed to abrogate Ts activity (priming with GT-MBSA and CY injection), nor could GT-primed cells be shown to inhibit the development or elicitation of GT-specific CMI in GAT-primed mice during the afferent and/or efferent stages of DTH. Our results suggest that GT nonresponsiveness does not result from the absence of GT-specific T cells or preferential induction of Ts. The results are discussed in the context of hole-in-the-repertoire and antigen presentation (determinant selection) models of Ir gene control.
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  • 10
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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