Abstract
B cells are susceptible to Fas ligand (FasL)+ CD4(+) Th1 cell-mediated apoptosis. We demonstrate that blocking the interactions between lymphocyte function associated (LFA)-1 and intercellular adhesion molecule(ICAM)-1 and ICAM-2 completely suppresses Fas-dependent B cell lysis. Antibodies to CD2 and CD48 partially suppress B cell apoptosis, whereas anti-B7.1 and anti-B7.2 antibodies have no effect. Also, B cells from ICAM-1-deficient mice are resistant to FasL+ T cell-mediated death. Our results suggest that LFA-1/ICAM interactions are crucial for Th1 cell-mediated B cell apoptosis and may contribute to the maintenance of B cell homeostasis in vivo.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Sequence
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Animals
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Antibodies / immunology
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Antigens, CD / immunology
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Antigens, CD / metabolism
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Apoptosis*
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B-Lymphocytes / cytology*
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Cell Adhesion Molecules / metabolism*
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Cell Line
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Chromium Isotopes
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Cytotoxicity, Immunologic
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Flow Cytometry
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Intercellular Adhesion Molecule-1 / metabolism
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Lymphocyte Function-Associated Antigen-1 / metabolism*
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Mice
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Mice, Inbred Strains
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Mice, Knockout
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Molecular Sequence Data
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Th1 Cells / immunology
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Th1 Cells / physiology*
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fas Receptor / immunology
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fas Receptor / metabolism
Substances
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Antibodies
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Antigens, CD
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Cell Adhesion Molecules
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Chromium Isotopes
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ICAM2 protein, human
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Lymphocyte Function-Associated Antigen-1
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fas Receptor
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Intercellular Adhesion Molecule-1