Abstract
Minimal numbers of CD8^+^ T cells are found in bronchoalveolar lavage (BAL) populations recovered from Sendai virus‐infected mice that are homozygous (−/−) for β2‐microglobulin (β2‐m) gene disruption. The prevalence of the CD8^+^ set was substantially increased in the pneumonic lungs of 8−12‐week radiation chimeras made using substantially class I major histocompatibility complex (MHC) glycoprotein‐negative β2‐m (−/−) recipients and normal β2‐m (+/+) bone marrow. Even so, the CD8^+^ (but not the CD4^+^) lymphocyte counts were still much lower than in the (+/+)→(+/+) controls. The (+/+)→(+/+) and (+/+)→(−/−) chimeras cleared Sendai virus and potent virus‐immune CD8^+^ cytotoxic T lymphocytes (CTL) specific for H‐2K^b^ + viral nucleoprotein peptide were found in the BAL from both groups. However, following in vivo depletion of the CD4^+^ population, only the (+/+)→(+/+) mice were able to deal with the infection. Similarly, adoptively transferred, H‐2K^b^‐restricted CD8^+^ T cells from previously‐primed (+/+) mice also failed to clear virus from the lungs of (+/+)→(−/−) chimeras infected within 2 weeks of reconstitution with bone marrow, though they were effective in the (+/+)→(+/+) controls. Sendai virus‐immune CD8^+^ T cells are thus unable to eliminate virus‐infected β2‐m (−/−) lung epithelial cells that might be thought to be expressing very small amounts of either isolated class I heavy chain, or class I MHC glycoprotein that has bound β2‐m derived from β2‐m (+/+) T cells or macrophages present in the pneumonic lung. Furthermore, the CD8^+^ CTL that are being exposed to β2‐m (+/+) stimulators in the BAL population cannot operate in some bystander mode to clear virus from respiratory epithelium.