Extent of gamma delta T cell involvement in the pneumonia caused by Sendai virus.
The prevalence of gamma delta 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 TCR gamma mRNA. The surface gamma delta 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 C gamma 1/2 and C gamma 4; the C-regions were utilized for productive TCR gene rearrangement. Sorting the lymphocytes from the BAL established that greater than 90% of both the TCR gamma and TCR beta mRNA partitioned to cells with the appropriate surface TCR phenotype, while less than 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 gamma delta TCR+ and TCR gamma mRNA+ cells were increased in mice depleted of alpha beta T cells by in vivo treatment with mAbs to CD4 and CD8, indicating that the CD4+ and CD8+ alpha beta and CD4-8- gamma delta T cell subsets may operate independently in this virus disease. The C gamma 1/2 mRNA phenotype predominated throughout the course of the active infection, with a transition to maximal prevalence of the C gamma 4 mRNA+ set occurring very late (Day 20) in the resolving inflammatory process. Large numbers of macrophages expressing mRNA (greater than 50%) for a mammalian 65-kDa heat shock protein (hsp65), a possible target for some of the gamma delta T cells, were present early (Days 5-7) and remained at lower levels (less than 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 gamma delta T cells are a minority of the infiltrating lymphocytes in Sendai virus pneumonia and provide new insights into the spectrum of hsp65 mRNA and TCR gamma mRNA expression during an inflammatory process.
Hou
S
S
St. Jude Children's Research Hospital, Memphis, Tennessee 38105.
Katz
J M
JM
Doherty
P C
PC
Carding
S R
SR
D000818:Animals; D015704:CD4 Antigens / Q000032:analysis; D016827:CD8 Antigens / Q000032:analysis; D005260:Female; D006360:Heat-Shock Proteins / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D010222:Parainfluenza Virus 1, Human; D018184:Paramyxoviridae Infections / Q000276:immunology*; D011014:Pneumonia / Q000276:immunology*; D012333:RNA, Messenger / Q000032:analysis; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000032:analysis* / Q000235:genetics; D013601:T-Lymphocytes / Q000502:physiology*
D015704:CD4 Antigens; D016827:CD8 Antigens; D006360:Heat-Shock Proteins; D012333:RNA, Messenger; D016692:Receptors, Antigen, T-Cell, gamma-delta