Document Detail


Induction of B cell apoptosis by TH0, but not TH2, CD4+ T cells.
MedLine Citation:
PMID:  7860739     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
X He; W Zhong; J J Goronzy; C M Weyand
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  95     ISSN:  0021-9738     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  1995 Feb 
Date Detail:
Created Date:  1995-03-20     Completed Date:  1995-03-20     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  564-70     Citation Subset:  AIM; IM    
Affiliation:
Division of Rheumatology, Mayo Clinic and Foundation, Rochester, Minnesota 55905.
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MeSH Terms
Descriptor/Qualifier:
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:
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

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