| Induction of B cell apoptosis by TH0, but not TH2, CD4+ T cells. | |
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MedLine Citation:
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PMID: 7860739 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Engagement of the T cell receptor molecules with MHC-antigen complexes presented by B cells ascertains antigen specificity in T cell-dependent help. Ligation of MHC molecules on the surface of B cells, however, has not only been implicated in antigen-specific T-B cell interaction, but has also been linked to the induction of B cell apoptosis. To examine the role of T helper cells in either induction of immunoglobulin synthesis or B cell apoptotic death, we have facilitated T cell receptor-MHC interaction through a bacterial superantigen. CD4+ T cell clones could be categorized into two clearly distinct subsets based upon their ability to promote B cell help in the presence of superantigen. One subset of T cell clones supported immunoglobulin synthesis, and thus functioned as effective helper cells. B cells interacting with the second subset of T cells did not differentiate into antibody-secreting cells, but underwent apoptosis. Both types of helper cells were able to provide contact help after anti-CD3 stimulation. Induction of apoptosis was a dominant phenomenon; the addition of the superantigen suppressed immunoglobulin production in B cells activated by anti-CD3-stimulated helper T cells, indicating that the T cells delivered an apoptotic signal to the B cell. T cell clones providing effective MHC restrictive B cell help could be distinguished from T cells facilitating B cell apoptosis based on their lymphokine secretion profile. Induction of B cell apoptosis was a feature of T cells with a TH0 lymphokine pattern. Promotion of MHC-restricted B cell help was associated with a TH2 lymphokine profile. TH1-derived cytokines alone could not substitute for apoptosis-inducing T cells. |
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Authors:
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X He; W Zhong; J J Goronzy; C M Weyand |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: The Journal of clinical investigation Volume: 95 ISSN: 0021-9738 ISO Abbreviation: J. Clin. Invest. Publication Date: 1995 Feb |
Date Detail:
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Created Date: 1995-03-20 Completed Date: 1995-03-20 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 7802877 Medline TA: J Clin Invest Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 564-70 Citation Subset: AIM; IM |
Affiliation:
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Division of Rheumatology, Mayo Clinic and Foundation, Rochester, Minnesota 55905. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Antigens, CD
/
immunology,
physiology Antigens, CD3 / immunology, physiology Apoptosis / drug effects, immunology* B-Lymphocytes / drug effects, immunology, physiology* CD4-Positive T-Lymphocytes / drug effects, physiology* Cell Communication / immunology Clone Cells Cytokines / pharmacology* HLA-DR Antigens / immunology Humans Interferon-gamma / biosynthesis Interferon-gamma, Recombinant / pharmacology Interleukin-2 / biosynthesis, pharmacology Interleukin-4 / biosynthesis, pharmacology Lymphocyte Activation* Major Histocompatibility Complex Receptors, Antigen, T-Cell / immunology T-Lymphocyte Subsets / immunology Tumor Necrosis Factor-alpha / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD; 0/Antigens, CD3; 0/Cytokines; 0/HLA-DR Antigens; 0/Interferon-gamma, Recombinant; 0/Interleukin-2; 0/Receptors, Antigen, T-Cell; 0/Tumor Necrosis Factor-alpha; 207137-56-2/Interleukin-4; 82115-62-6/Interferon-gamma |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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