THE ROLE OF GAMMA-DELTA T-LYMPHOCYTES IN LIPOPOLYSACCHARIDE-INDUCED EOSINOPHIL ACCUMULATION INTO THE MOUSE PLEURAL CAVITY

LPS induces an accumulation of eosinophils in the pleural cavity that requires resident macrophages and lymphocytes, but is independent of I L-5 production. In the present study we investigated the involvement o f different T lymphocyte subsets on the modulation of LPS-induced eosi nophil accumulation into the pleural cavity of mice. Within 4 h after LPS injection the number of neutrophils in the pleural cavity increase d significantly. Mononuclear cell counts increased after 12 h, while a significant rise on eosinophil counts was observed only after 24 h. T lymphocytes counts were increased in the pleural cavity 24 and 48 h a fter LPS administration. This T lymphocyte accumulation was accounted for by an influx of the gamma delta(+) subset, while CD4(+) and CD8(+) subsets did not accumulate in the pleural cavity after LPS stimulatio n. All those changes had resolved 96 h after LPS injection, Depletion of T lymphocytes by treatment with mAb anti-Thy 1.0 inhibited the eosi nophil accumulation triggered by LPS. Aiming to clarify which T lympho cyte subset would be involved in the LPS-induced eosinophil accumulati on, we depleted mice of various T lymphocyte subpopulations using spec ific Abs. Depletion of either CD4(+) or CD8(+) subsets failed to inhib it LPS-induced eosinophil migration. In contrast, when mice were treat ed with anti-gamma delta(+) T lymphocyte mAb, a significant reduction of LPS-induced eosinophil accumulation was observed. Similarly, the ad ministration of LPS in BALB/c-nu/nu mice induced the expected signific ant influx of eosinophils into the pleural cavity. Our results indicat e that the gamma delta(+) T lymphocytes are centrally involved in LPS- induced eosinophil accumulation in mice.