HOST RESPONSE TO SENDAI VIRUS IN MICE LACKING CLASS-II MAJOR HISTOCOMPATIBILITY COMPLEX GLYCOPROTEINS

The development of Sendai virus-specific cytotoxic T-lymphocyte (CTL) effecters and precursors (CTLp) has been compared for mice that are ho mozygous (-/-) for a disruption of the H-2I-A(b) class II major histoc ompatibility complex glycoprotein and for normal (+/+) controls. The g eneration of CD8(+) CTLp was not diminished in the -/- mice, though th ey failed to make virus-specific immunoglobulin G class antibodies. Wh ile the cellularity of the regional lymph nodes was decreased, the inf lammatory process assayed by bronchoalveolar lavage (BAL) of the pneum onic lung was not modified, and potent CTL effecters were present in B AL populations recovered from both groups at day 10 after infection. T here was little effect on virus clearance. Production of interleukin-2 by both freshly isolated BAL inflammatory cells and cultured lymph no de cells was greatly diminished, though the -/- mice still made substa ntial levels of gamma interferon. However, treating the mice with a si ngle 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-2(b) mice, the development of Se ndai virus-specific CD8(+) T cell-mediated immunity is not compromised by the absence of a concurrent class II major histocompatibility comp lex-restricted response.