The prevalence of γδ T cells in bronchoalveolar lavage (BAL) populations recovered from the respiratory tract of young, adult C57BL/6J mice infected intranasally (i.n.) with Sendai virus has been assessed by FACS-phenotyping, and by probing cytocentrifuge preparations for expression of TCRγ mRNA. The surface γδ TCR+ set comprised from 5 to 20% of the inflammatory lymphocytes in sequential samples taken throughout the course of this nonfatal viral pneumonia. The BAL population also contained numerous cells expressing mRNA for Cγ 1/2 and Cγ4; the C-regions were utilized for productive TCR gene rearrangement. Sorting the lymphocytes from the BAL established that >90% of both the TCRγ and TCRβ mRNA partitioned to cells with the appropriate surface TCR phenotype, while <7% of the TCR mRNA+ cells in the total inflammatory exudate were phagocytes that engulfed latex particles. Both the frequency and the total numbers of the γδ TCR+ and TCRγ mRNA+ cells were increased in mice depleted of αβ T cells by in vivo treatment with mAbs to CD4 and CD8. indicating that the CD4+ and CD8+ αβ and CD4-8- γδ T cell subsets may operate independently in this virus disease. The Cγl/2 mRNA phenotype predominated throughout the course of the active infection, with a transition to maximal prevalence of the Cγ4 mRNA+ set occurring very late (Day 20) in the resolving inflammatory process. Large numbers of macrophages expressing mRNA (>50%) for a mammalian 65-kDa heat shock protein (hsp65), a possible target for some of the γδ T cells, were present early (Days 5-7) and remained at lower levels (<20%) thereafter. These hsp65 mRNA+ macrophages were much less apparent in BAL populations from mice depleted concurrently of the CD4+ and CD8+ T cell subsets, indicating that exposure to Sendai virus alone is not the major factor inducing the transcription of this endogenous gene. These experiments thus establish that γδ T cells are a minority of the infiltrating lymphocytes in Sendai virus pneumonia and provide new insights into the spectrum of hsp65 mRNA and TCRγ mRNA expression during an inflammatory process. © 1992.