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  • 1
    Publication Date: 2019
    Description: 〈p〉Immunoglobulin E (IgE), a key mediator in allergic diseases, is spontaneously elevated in mice with disrupted commensal microbiota such as germ-free (GF) and antibiotics-treated mice. However, the underlying mechanisms for aberrant IgE elevation are still unclear. Here, we demonstrate that food antigens drive spontaneous IgE elevation in GF and antibiotics-treated mice by generating T helper 2 (T〈sub〉H〈/sub〉2)–skewed T follicular helper (T〈sub〉FH〈/sub〉) cells in gut-associated lymphoid tissues (GALTs). In these mice, depriving contact with food antigens results in defective IgE elevation as well as impaired generation of T〈sub〉FH〈/sub〉 cells and IgE-producing cells in GALT. Food antigen–driven T〈sub〉FH〈/sub〉 cells in GF mice are mostly generated in early life, especially during the weaning period. We also reveal that food antigen–driven T〈sub〉FH〈/sub〉 cells in GF mice are actively depleted by colonization with commensal microbiota. Thus, our findings provide a possible explanation for why the perturbation of commensal microbiota in early life increases the occurrence of allergic diseases.〈/p〉
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-07-14
    Description: In typical immune responses, contact with antigen causes naive T cells to proliferate and differentiate into effector cells. After the pathogen is destroyed, most effector T cells are eliminated-thereby preserving the primary T cell repertoire-but some cells survive and form long-lived memory cells. During each stage of this process, the life or death fate of T cells is strictly regulated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sprent, J -- Tough, D F -- AG01743/AG/NIA NIH HHS/ -- AI21487/AI/NIAID NIH HHS/ -- AI46710/AI/NIAID NIH HHS/ -- CA38355/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2001 Jul 13;293(5528):245-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, IMM4, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. jsprent@scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11452113" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Death ; Cell Survival ; Cytokines/physiology ; *Immunologic Memory ; Infection/immunology ; T-Lymphocytes/*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
    Publication Date: 1999-11-05
    Description: Peptide-major histocompatibility complex protein complexes (pMHCs) on antigen-presenting cells (APCs) are central to T cell activation. Within minutes of peptide-specific T cells interacting with APCs, pMHCs on APCs formed clusters at the site of T cell contact. Thereafter, these clusters were acquired by T cells and internalized through T cell receptor-mediated endocytosis. During this process, T cells became sensitive to peptide-specific lysis by neighboring T cells (fratricide). This form of immunoregulation could explain the "exhaustion" of T cell responses that is induced by high viral loads and may serve to down-regulate immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, J F -- Yang, Y -- Sepulveda, H -- Shi, W -- Hwang, I -- Peterson, P A -- Jackson, M R -- Sprent, J -- Cai, Z -- New York, N.Y. -- Science. 1999 Oct 29;286(5441):952-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉R. W. Johnson Pharmaceutical Research Institute, 3210 Merryfield Row, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10542149" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Drosophila ; *Endocytosis ; Flow Cytometry ; Histocompatibility Antigens/*immunology ; Macromolecular Substances ; Peptides/*immunology ; Receptors, Antigen, T-Cell/*immunology ; Recombinant Fusion Proteins/genetics/immunology ; T-Lymphocytes/*immunology/metabolism ; T-Lymphocytes, Cytotoxic/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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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-06-15
    Description: The specificity of mature CD8+ and CD4+ T lymphocytes is controlled by major histocompatibility complex (MHC) class I and class II molecules, respectively. The MHC class specificity of T cells is stringent in many assays, but is less evident when cells are supplemented with exogenous lymphokines. The repertoire of T cells is shaped through contact with MHC molecules in the thymus and involves a complex process of positive selection and negative selection (tolerance). Tolerance of immature T cells to MHC molecules can reflect either clonal deletion or anergy and results from intrathymic contact with several cell types, including epithelial cells and cells with antigen-presenting function. Unlike immature T cells, mature T cells are relatively resistant to tolerance induction. In certain situations partial unresponsiveness of mature T cells can be achieved by exposing T cells to foreign MHC molecules expressed on atypical antigen-presenting cells. Tolerance is rarely complete, however, and the precise requirements for tolerizing mature T cells are still unclear.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sprent, J -- Gao, E K -- Webb, S R -- AI21487/AI/NIAID NIH HHS/ -- CA25803/CA/NCI NIH HHS/ -- CA38355/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 15;248(4961):1357-63.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Research Institute of Scripps Clinic, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1694041" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Presenting Cells/immunology ; Bone Marrow/immunology ; CD4-Positive T-Lymphocytes/immunology ; Clone Cells/immunology ; Epitopes/immunology ; Histocompatibility Antigens/*immunology ; Histocompatibility Antigens Class II/immunology ; *Immune Tolerance ; *Immunity ; Interleukin-2/physiology ; Mice ; Mice, Transgenic ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Regulatory/immunology ; Thymus Gland/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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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-06-29
    Description: Antigen-specific tolerance of T cells to minor lymphocyte stimulatory (Mls) antigens can be induced in mice by neonatal injection of foreign lymphohematopoietic cells. Although immune responses to Mlsa antigens are controlled by B cells, CD8+ T cells were the most effective cell type for induction of Mlsa tolerance. Tolerance was evident in both thymus and lymph nodes and could be induced by as few as 2 x 10(4) CD8+ T cells; these cells were 50 to 100 times as potent as CD4+ cells or B cells in causing functional tolerance and deletion of V beta 6+ T cells. Thus, intrathymic contact with antigens expressed on CD8+ T cells may play an important role in controlling the normal development of tolerance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Webb, S R -- Sprent, J -- CA 25803/CA/NCI NIH HHS/ -- CA 38355/CA/NCI NIH HHS/ -- CA 41993/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 29;248(4963):1643-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Research Institute of Scripps Clinic, La Jolla 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1973003" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Antigens, CD8 ; Antigens, Differentiation, T-Lymphocyte/*immunology ; Antigens, Surface/*immunology ; B-Lymphocytes/immunology ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/immunology ; *Immune Tolerance ; Lymphocyte Depletion ; Mice ; Mice, Inbred Strains ; Minor Lymphocyte Stimulatory Antigens ; Receptors, Antigen, T-Cell/immunology ; Spleen/immunology ; T-Lymphocytes/*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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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1996-06-28
    Description: T cell proliferation in vivo is presumed to reflect a T cell receptor (TCR)-mediated polyclonal response directed to various environmental antigens. However, the massive proliferation of T cells seen in viral infections is suggestive of a bystander reaction driven by cytokines instead of the TCR. In mice, T cell proliferation in viral infections preferentially affected the CD44hi subset of CD8+ cells and was mimicked by injection of polyinosinic-polycytidylic acid [poly(I:C)], an inducer of type I interferon (IFN I), and also by purified IFN I; such proliferation was not associated with up-regulation of CD69 or CD25 expression, which implies that TCR signaling was not involved. IFN I [poly(I:C)]-stimulated CD8+ cells survived for prolonged periods in vivo and displayed the same phenotype as did long-lived antigen-specific CD8+ cells. IFN I also potentiated the clonal expansion and survival of CD8+ cells responding to specific antigen. Production of IFN I may thus play an important role in the generation and maintenance of specific memory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tough, D F -- Borrow, P -- Sprent, J -- AI21487/AI/NIAID NIH HHS/ -- CA25803/CA/NCI NIH HHS/ -- CA38355/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1996 Jun 28;272(5270):1947-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8658169" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/analysis ; Antigens, CD44/analysis ; Antigens, Differentiation, T-Lymphocyte/analysis ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/cytology/*immunology ; Cell Division ; Cell Survival ; Immunologic Memory ; Immunophenotyping ; Interferon Type I/*immunology/pharmacology ; Lectins, C-Type ; *Lymphocyte Activation ; Lymphocytic Choriomeningitis/*immunology ; Lymphocytic choriomeningitis virus/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Poly I-C/pharmacology ; Receptors, Antigen, T-Cell/immunology ; Receptors, Interleukin-2/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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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1994-09-02
    Description: Differentiation of immature T and B cells in the primary lymphoid organs gives rise to a pool of long-lived lymphocytes that recirculate through the secondary lymphoid tissues. On the basis of their surface markers, T and B cells comprise a mixture of naive and memory cells with differing life-spans. Immunization (and vaccination) causes naive lymphocytes to proliferate and differentiate into effector cells and memory cells. Whether the survival of memory cells is innate or requires persistent contact with residual antigen is controversial. Resolving this issue may be crucial for designing optimal vaccines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sprent, J -- Tough, D F -- AI21487/AI/NIAID NIH HHS/ -- CA25803/CA/NCI NIH HHS/ -- CA38355/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Sep 2;265(5177):1395-400.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8073282" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*immunology ; B-Lymphocytes/cytology/*immunology ; Cell Differentiation ; Cell Survival ; Humans ; Immunization ; Immunologic Memory/*immunology ; Lymphoid Tissue/cytology/immunology ; T-Lymphocytes/cytology/*immunology ; Vaccines/*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: 2006-02-18
    Description: Interleukin-2 (IL-2), which is a growth factor for T lymphocytes, can also sometimes be inhibitory. Thus, the proliferation of CD8+ T cells in vivo is increased after the injection of a monoclonal antibody that is specific for IL-2 (IL-2 mAb), perhaps reflecting the removal of IL-2-dependent CD4+ T regulatory cells (T regs). Instead, we show here that IL-2 mAb augments the proliferation of CD8+ cells in mice simply by increasing the biological activity of preexisting IL-2 through the formation of immune complexes. When coupled with recombinant IL-2, some IL-2/IL-2 mAb complexes cause massive (〉100-fold) expansion of CD8+ cells in vivo, whereas others selectively stimulate CD4+ T regs. Thus, different cytokine-antibody complexes can be used to selectively boost or inhibit the immune response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boyman, Onur -- Kovar, Marek -- Rubinstein, Mark P -- Surh, Charles D -- Sprent, Jonathan -- New York, N.Y. -- Science. 2006 Mar 31;311(5769):1924-7. Epub 2006 Feb 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, IMM4, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484453" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Antibodies, Monoclonal/*immunology/pharmacology ; Antigen-Antibody Complex/*immunology ; CD8-Positive T-Lymphocytes/cytology/*immunology ; Cell Proliferation ; Enzyme-Linked Immunosorbent Assay ; Immunologic Memory ; Interleukin-2/*immunology/pharmacology ; Interleukin-4/immunology ; *Lymphocyte Activation ; Lymphocyte Count ; Mice ; Mice, Inbred C57BL ; Receptors, Interleukin-2/analysis/immunology/metabolism ; Recombinant Proteins/pharmacology ; T-Lymphocyte Subsets/cytology/*immunology ; T-Lymphocytes, Regulatory/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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  • 9
    Publication Date: 2006-07-19
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 10
    Publication Date: 2004-06-14
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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