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J Immunol ; 165(10): 5387-91, 2000 Nov 15.
Article in English | MEDLINE | ID: mdl-11067887

ABSTRACT

Although they are known for their capacity to kill infected cells, Ag-specific CD8(+) T cells elaborate other effector mechanisms, including TNF and IFN-gamma, that contribute to defense against infection. Ag-specific CD8(+) T cells rapidly turn ON and turn OFF IFN-gamma production in direct response to Ag contact, presumably to minimize the potential immunopathology that could result from inappropriate secretion of this inflammatory mediator. In this study, we show, using in vitro propagated and directly ex vivo-analyzed Ag-specific CD8(+) T cells, that in contrast to Ag-dependent ON/OFF cycling of IFN-gamma production, the cessation of TNF production by the same IFN-gamma producing cells is rapid and Ag independent.


Subject(s)
Antigens, T-Independent/physiology , CD8-Positive T-Lymphocytes/immunology , CD8-Positive T-Lymphocytes/metabolism , Epitopes, T-Lymphocyte/immunology , Tumor Necrosis Factor-alpha/biosynthesis , Animals , Antigens, Bacterial/immunology , Bacterial Proteins/immunology , Cell Line , Immunity, Cellular , Interferon-gamma/biosynthesis , Kinetics , Listeriosis/immunology , Lymphocytic Choriomeningitis/immunology , Lymphocytic choriomeningitis virus/immunology , Mice , Mice, Inbred BALB C , T-Lymphocyte Subsets/immunology , T-Lymphocyte Subsets/metabolism , Tumor Cells, Cultured
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