Mycobacterium avium-intracellulare complex (MAC) consists of 28 serotypes. Co-infectionof several specific serotype strains with the advent of acquired immunodeficiencysyndrome (AIDS) has been dramatically increasing in the past fifteen years, although thereason for this fact is not clearly understood. Since the cell surface lipid components of MAC impaired the capacity of human peripheral blood mononuclear cells (PBMC) to proliferate, some particular glycopeptidolipid (GPL) with serologically specific carbohydratechains are supposed to inhibit blastogenesis and to affect the immune response in MACinfection. In this study, we have investigated the effect of serovar 4 and 16GPLs on thehuman PBMC function and cell mediated immunity. As the result, it was demonstratedthat the percentage of viable cells was decreased prominently after the incubation of PBMC with the serovar 4 GPL. Blastogenic responses of PBMC to stimulation with thepurified protein derivatives (PPD) were inhibited by the presence of GPL dosedependently.In the case of stimulation with anti-CD3 antibody (a-CD3 Ab), blastogenicresponse of PBMC was suppressed markedly by GPL at the concentration of 175μg/m
l. Flow-cytometric analysis demonstrated that the expression of interleukin-2 receptor alphaon a-CD3 Ab-stimulated T lymphocyte was markedly inhibited in the presence of GPL. Enzyme-linked immunosorbent assay showed that the production of interleukin-2 by a-CD3 Ab-stimulated PBMC was reduced dose-dependently after the incubation of PBMC with GPL. In these results, there was no remarkable difference between serovar 4 andserovar 16 GPLs. These results indicate that serovar 4 and 16 GPLs inhibit the cell mediatedimmunity and serovar 4 GPL can affect the viability of PBMC.
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