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 beta2-microglobulin-deficient [1beta2-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 beta2-m (+/+) mice, though inflammatory CD4+ T cells from both beta2-m (-/-) and beta2-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 132-m (-/-) mice are potent inducers of apoptosis, while this is not the case for the 132-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.