A KINETIC COMPARATIVE-STUDY ON LYMPHOCYTE-RESPONSES TO SUPERANTIGEN AND PHYTOHEMAGGLUTININ - RECIPROCAL PRESENTATION OF SUPERANTIGEN ON THESURFACE OF ACTIVATED LYMPHOCYTES

The kinetics of thymidine incorporation into fractionated T lymphocyte s responding to bacterial super-antigens were compared to those of cel ls activated by phytohemagglutinin (PMA), Evident differences between the kinetics of cell proliferation induced by PHA-P and staphylococcal enterotoxin B (SEE) emerged after Day 4 of culture, PHA-P-induced pro liferative responses of peripheral blood mononuclear cells (PBMCs) and fractionated cells were apparent on Day 4 because of the presence of accessory cells in the initial cell suspensions. This gradually dimini shed in correlation with the decline of accessory cells in the culture s. The SEE-induced cell growth (PBMCs and CD4(+) cells), however, cont inued until Day 9 of the culture, This finding suggests the reciprocal usage of MMC class II molecules to present SEE by activated T lymphoc ytes for superantigen-induced T cell activation and suggests that supe rantigen-related immune activation may depend in part on the potential of activated T lymphocytes to mediate reciprocal cell-to-cell interac tions in the presence of superantigens. The decline observed in the CD 8(+) cell response to SEE and toxic shock syndrome toxin-l after Day 4 was revived by exogenous recombinant interleukin-2 (rIL-2) supplement ation, suggesting that the consequent autocrine or paracrine secretion of IL-2 from the responding cells is essential for subsequent cell pr oliferation, SEE-induced cell proliferation was significantly suppress ed by anti-CD11a (lymphocyte function-associated antigen-1; LFA-I, alp ha-Chain) monoclonal antibody, and the inhibitory effect was most obvi ous in 6-day cultured CD8(+) lymphocytes. The results suggest that the lymphocyte response associated with the ceIl-to- cell copresentation of superantigens involves LFA-1 molecules as an accessory factor, part icularly ill CD8(+) lymphocytes. (C) Academic Press, Inc.