PULMONARY LYMPHOCYTE RECRUITMENT - DEPLETION OF CD8-CELLS DOES NOT IMPAIR THE PULMONARY IMMUNE-RESPONSE TO INTRATRACHEAL ANTIGEN( T)

CD8+ T cells predominate in die lungs in hypersensitivity and human im munodeficiency virus-related lymphocytic pneumonitis, but their role i n the immunopathogenesis of lung disease is unknown. We have shown tha t in immunized mice depleted of CD4+ T cells, CD8+ T cells are recruit ed into the lungs in response to intratracheal antigen challenge with sheep red blood cells (SRBC) (J. Clin. Invest. 1991; 88:1244-1254) or to pulmonary infection with Pneumocystis carinii (Am. J Respir. Cell M ol. Biol. 1991; 5:186-197), suggesting that recruitment of CD8+ T cell s does not depend on CD4+ T cell-derived signals. Because CD8+ T cells themselves produce a variety of chemotactic and immunoregulatory cyto kines, CD8+ T cells may be important participants in, and modulators o f, pulmonary immune responses. To test this hypothesis, we examined th e effects of CD8+ T cell depletion on the generation of a pulmonary im mune response in vivo. We monitored the recruitment of mononuclear cel ls into lungs in the absence of CD8-dependent signals and measured the duration of pulmonary inflammation in the absence of suppressor CD8T cells. Primed mice were treated with anti-CD8 monoclonal antibody to deplete CD8+ T cells and subsequently were challenged intratracheally with 5 x 10(8) SRBC. At various times after challenge, total and diff erential cell counts and lymphocyte phenotypes were measured in bronch oalveolar lavage fluid by flow cytometry and lungs were scored histolo gically. We found that depletion of CD8+ T cells neither decreased rec ruitment of immune and inflammatory cells nor prolonged the pulmonary immune response. We conclude that: (1) CD8+ T cells do not produce sig nals necessary for cellular recruitment to the lungs in response to th is particulate MHC class II-restricted antigen, and (2) termination of this pulmonary immune response does not require the action of CD8+ T cells. These results indicate that CD8+ T cells do not play a signific ant role in either the generation or the modulation of pulmonary immun e responses to SRBC antigens.