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  • 1
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    Visualization of specific B and T lymphocyte interactions in the lymph node (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Different B cell populations mediate early and late memory during an endogenous immune response (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 3
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    Naive and memory CD4+ T cell survival controlled by clonal abundance (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 4
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    Humoral immunity. Apoptosis and antigen affinity limit effector cell differentiation of a single naive B cell (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Most microbe-specific naive CD4(+) T cells produce memory cells during infection (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 6
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    Effects of cyclosporine A on T cell development and clonal deletion (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Published by American Association for the Advancement of Science (AAAS)
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