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Characterization and function of CD3+ CD4- CD8- TcR-alpha beta bearing cells infiltrating the lung during the immune
J C Chang1, L Zhang, S G Distler
1Department of Microbiology and Immunology, University of Kentucky Medical Center, Lexington 40536-0084.
To analyze immunological reactivity within the lung, we have examined the cellular changes in the lung during an experimentally induced immune response. When mice, primed intraperitoneally, were challenged intratracheally (i.t.), there was an increase in the total cells recovered from the lung as well as in the percent of Thyl+ cells, L3T4+ cells, and macrophages. More interesting was the observation that 40 to 60% of the CD3+ cells infiltrating the lung were CD4- CD8- and cells of this phenotype were not found in the tracheobronchial lymph node draining the lung. About 40% of the double negative T (DNT) cells bore TcR-alpha beta, and in vitro clones of the same phenotype, established from the i.t. challenged lungs, were shown, upon ConA stimulation, to synthesize mRNA for IL-2, IL-3, IL-4, IL-5, IL-6, IFN gamma, TNF alpha, GM-CSF, TGF beta but not of IL-1 or EGF. Functionally, the double negative T cell clones suppressed the antigen-stimulated proliferative response of TH1 clones in vitro, which suggests that they may be involved in the down-regulation of antigen-initiated inflammatory responses in vivo.
To analyze immunological reactivity within the lung, we have examined the cellular changes in the lung during an experimentally induced immune response. When mice, primed intraperitoneally, were challenged intratracheally (i.t.), there was an increase in the total cells recovered from the lung as well as in the percent of Thyl+ cells, L3T4+ cells, and macrophages. More interesting was the observation that 40 to 60% of the CD3+ cells infiltrating the lung were CD4- CD8- and cells of this phenotype were not found in the tracheobronchial lymph node draining the lung. About 40% of the double negative T (DNT) cells bore TcR-alpha beta, and in vitro clones of the same phenotype, established from the i.t. challenged lungs, were shown, upon ConA stimulation, to synthesize mRNA for IL-2, IL-3, IL-4, IL-5, IL-6, IFN gamma, TNF alpha, GM-CSF, TGF beta but not of IL-1 or EGF. Functionally, the double negative T cell clones suppressed the antigen-stimulated proliferative response of TH1 clones in vitro, which suggests that they may be involved in the down-regulation of antigen-initiated inflammatory responses in vivo.