Divergence between cytotoxic effector function and tumor necrosis factor alpha production for inflammatory CD4+ T cells from mice with Sendai virus pneumonia.
Sendai virus pneumonia in beta 2-microglobulin-deficient [beta 2-m(-/-)] mice lacking CD8+ T cells is characterized by the development of CD4+ cytotoxic T lymphocytes that can be recovered directly from the respiratory tract. These CD4+ cytotoxic T lymphocytes are not found in beta 2-m (+/+) mice, though inflammatory CD4+ T cells from both beta 2-m (-/-) and beta 2-m (+/+) mice produce substantial amounts of tumor necrosis factor alpha. Blocking experiments with a monoclonal antibody that also inhibits tumor necrosis factor beta show that the secreted forms of these two cytokines are not responsible for virus-specific killing of class II major histocompatibility complex-compatible targets. Comparison of electron micrographs indicates that the CD4+ effectors from the beta 2-m (-/-) mice are potent inducers of apoptosis, while this is not the case for the beta 2-m (+/+) CD4+ set. These experiments further define the functional status of virus-specific CD4+ T cells responding in vivo in the presence or absence of CD8+ effectors.
Department of Immunology, St. Judge Children's Research Hospital, Memphis, Tennessee 38105.
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Hou
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Fishman
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Murti
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PC
Doherty
D000818:Animals; D015704:CD4 Antigens / Q000032:analysis / Q000276:immunology*; D002448:Cell Adhesion; D002478:Cells, Cultured; D003602:Cytotoxicity, Immunologic; D015395:Histocompatibility Antigens Class I / Q000235:genetics / Q000276:immunology; D007249:Inflammation; D051379:Mice; D008854:Microscopy, Electron; D010222:Parainfluenza Virus 1, Human / Q000276:immunology*; D018184:Paramyxoviridae Infections / Q000276:immunology*; D011024:Pneumonia, Viral / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000382:microbiology / Q000648:ultrastructure; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*
D015704:CD4 Antigens; D015395:Histocompatibility Antigens Class I; D014409:Tumor Necrosis Factor-alpha