engleski

Involvement of T cells in upregulation of hepatic MHC class II expression in mice treated with PGM-Zn

In several models it has been shown that peptidoglycan monomer (PGM), originally prepared by biosynthesis from culture fluids of penicillin-treated Brevibacterium divaricatum, has marked immunomodulating properties. However, in some experimentally or naturally occurring states of immunosuppression (halothane anesthesia, obstructive jaundice or aging) we obtained even better immunostimulation with new metal analogue of PGM, in which basic substance PGM was linked with Zn (PGM-Zn). Recently, we observed that its stimulatory effects on humoral immunity might be both-T-cell dependent (TD) and T-cells independent (TI), suggesting that PGM-Zn may enhance the co-stimulatory signals coming from the activated T cells, but may act also on mature B cells as polyclonal activator, without the T-cell help. To obtain more information about the mechanisms of action of PGM-Zn, in this work, we attempted to elucidate the role of T cells in activation of mononuclear phagocyte system, which frequently may be induced by PGM-Zn. For this purpose we followed up the hepatic MHC class II expression and phagocytic activity of peritoneal macrophages, in sheep red blood cell sensitized mice, which were in vivo depleted of CD4+, CD8+ or of both T cells subpopulation. Primary and secondary immune response was analyzed and the data were correlated with cellularity of bone marrow, thymus and spleen, and phenotypic profile of splenic cells. The results have shown that PGM-Zn induces significant hepatic upregulation of MHC class II expression and increased phagocytic activity of PEC. Depletion of CD4+ or CD4+CD8+ T cells, however, significantly lowered both of its activities, indicating that T cells and their cytokines have important role in PGM-Zn-induced immunostimulation.

PGM-Zn; CD4 and/or CD8-depletion; SRBC; humoral immunity

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