| Follicular exclusion and rapid elimination of hen egg lysozyme autoantigen-binding B cells are dependent on competitor B cells, but not on T cells. | |
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MedLine Citation:
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PMID: 9886397 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In mice with a diverse B cell repertoire, hen egg lysozyme (HEL) autoantigen-binding B cells are excluded from follicles and eliminated in 3 days. To explore the roles of competitor B cells and of T cells in this mechanism of self-tolerance, HEL-specific B cells were transferred into mice containing HEL and deficient in endogenous B cells (muMT), T cells (TCR-/-), or B and T cells (RAG1-/-). Previous studies suggested a dual requirement for B cell receptor (BCR) engagement and competition in HEL autoantigen-binding B cell elimination, but interpretation of these experiments has been confounded by the possible failure to independently regulate autoantigen concentration and competitor B cell frequency. In experiments in this study, we have fixed one variable, HEL concentration, while varying the second, the presence or absence of other B cells. By this approach, we find that follicular exclusion and rapid elimination of autoreactive B cells require BCR engagement plus competition with other B cells, rather than BCR engagement alone. We also find, by transfers into T cell-deficient mice, that T cells are not required for this peripheral tolerance mechanism. Unexpectedly, in mice lacking both T cells and competitor B cells (RAG1-/-), transferred HEL-binding cells survive less well than in mice just lacking competitor B cells. These results suggest T cells can enhance autoreactive B cell survival. Enhanced survival of autoreactive B cells, due to the presence of T cells and the lack of competitor B cells, might contribute to the elevated frequency of autoimmunity in B cell-deficient individuals. |
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Authors:
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K N Schmidt; J G Cyster |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: 162 ISSN: 0022-1767 ISO Abbreviation: J. Immunol. Publication Date: 1999 Jan |
Date Detail:
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Created Date: 1999-01-21 Completed Date: 1999-01-21 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 284-91 Citation Subset: AIM; IM |
Affiliation:
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Department of Microbiology and Immunology, University of California, San Francisco 94143, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Autoantigens / metabolism* B-Lymphocyte Subsets / immunology*, metabolism, pathology Binding, Competitive / immunology Cell Movement / immunology* Cell Survival / immunology Chickens Lymphoid Tissue / immunology*, metabolism, pathology Lymphopenia / genetics, immunology, pathology Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Muramidase / immunology*, metabolism T-Lymphocyte Subsets / immunology*, metabolism |
| Grant Support | |
ID/Acronym/Agency:
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AI 40098/AI/NIAID NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Autoantigens; EC 3.2.1.17/Muramidase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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