engleski

Modulatory effects of somatostatin on anti-CD3 and dexamethasone-induced apoptosis of murine thymocytes

Although it is well known that the thymic epithelium is the main cellular component in driving the maturation of thymocytes through cell-to-cell and extracellular matrix-mediated interactions, in the regulation of proliferation and differentiation of T cells seems to participate also the locally produced hormones and neuropeptides, which in an autocrine and paracrine manner influence the thymic functions. In an attempt to elucidate the role of somatostatin in these events, in this study we investigated in vivo and in vitro effects of long acting somatostatin analogue, SMS 201-995 (SMS), on dexamethasone (DEX) and activation (anti-CD3 monoclonal antibodies) induced apoptosis of thymocytes. The data were estimated by analysis of absolute cellularity, subdiploid peak of DNA and maturational stage of thymocytes, detecting the CD4 and/or CD8 and T cell receptor (TCR) expression on thymocytes. The results have shown that SMS, given in vivo may potentiate the early phase of DEX-induced nuclear fragmentation (at 24h), accelerating simultaneously the elimination of thymic cells with double positive (DP) CD4high CD8high phenotype (expressed both as percentage and absolute number). On the contrary, SMS, given both in vivo and in vitro, down-regulated the late process (at 72h) of nuclear fragmentation, induced by anti-CD3 mAb, minimizing, simultaneously, the elimination of DP cells (expressed both as percentage and absolute number), and retarding the TRC  / high expression on anti-CD3 triggered apoptotic cells. During the early phase of activation-induced apoptosis SMS, however, augmented the hypoplasia in thymus, enhancing simultaneously the decrease of absolute number of thymic DP cells in CD3-treated mice.

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