Host response to Sendai virus in mice lacking class II major histocompatibility complex glycoproteins.

The development of Sendai virus-specific cytotoxic T-lymphocyte (CTL) effectors and precursors (CTLp) has been compared for mice that are homozygous (-/-) for a disruption of the H-2I-Ab class II major histocompatibility complex glycoprotein and for normal (+/+) controls. The generation of CD8+ CTLp was not diminished in the -/- mice, though they failed to make virus-specific immunoglobulin G class antibodies. While the cellularity of the regional lymph nodes was decreased, the inflammatory process assayed by bronchoalveolar lavage (BAL) of the pneumonic lung was not modified, and potent CTL effectors were present in BAL populations recovered from both groups at day 10 after infection. There was little effect on virus clearance. Production of interleukin-2 by both freshly isolated BAL inflammatory cells and cultured lymph node cells was greatly diminished, though the -/- mice still made substantial levels of gamma interferon. However, treating the mice with a single dose of a monoclonal antibody to this cytokine, at least some of which is made by CD8+ T cells, did not decrease CTLp frequencies. As found previously with CD4-depleted H-2b mice, the development of Sendai virus-specific CD8+ T-cell-mediated immunity is not compromised by the absence of a concurrent class II major histocompatibility complex-restricted response.