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On the role of T lymphocytes in stimulation of humoral immunity and activation of macrophages 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). To obtain more information about the mechanisms of action of PGM-Zn, in this work, we attempted to elucidate the role of T cells on it's effects on humoral immunity and on activation of mononuclear phagocyte system. For this purpose we followed up the PFC generation, serum antibody production, hepatic MHC class II expression and phagocytic activity of peritoneal macrophages, in SRBC 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 stimulatory effects on humoral immunity and on the process of isotype switching might be both-T-cell dependent and T-cells independent, 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. Simultaneously we observed that PGM-Zn might induce significant hepatic upregulation of MHC class II expression and increase the phagocytic activity of peritoneal exudate cells. These effects were also markedly affected by depletion of CD4+ or both CD4+CD8+ T cells. Taken together the data emphasize the role of T cells and their cytokines in PGM-Zn-induced immunostimulation.

PGM-Zn; T-lymphocytes; hepatic MHC class II expression; humoral immunity

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