We have previously demonstrated that CD4+ anti-myelin basic protein (MBP) T cells protect hippocampal neurons against trimethyltin-induced damage. In this study, we employ immunocytochemicalmethods to investigate the infl uence of administration of T cells to the response of microglia and of NG2+ cells to TMT-induced damage. Female Lewis rats were treated with anti-MBP CD4+ T cells (4 million per animal, i.v.) 24 hours after TMT (8 mg/kg, i.p.) intoxication. TMT caused degeneration of CA4 hipppocampal neurons and evoked an abundant reaction of microglial and NG2+ cells in the injured zone. The number of activated cells increased about 4-fold relative to controls as assessed on the 21st day after TMT treatment. A bulk of the cells of ameboid morphology, which expressed NG2 or microglial antigens, appeared in the zone of neurodegeneration. Interestingly, many of the cells of ameboid phenotype shared both antigens. Administration of T cells downregulated the activation of both glial classes and considerably reduced the formation of the ameboid phenotype forms. The latter were decreased, on average, by 60 percent. Our data suggest that the diminished activation of microglia and NG2+ cells, particularly the decrease of the ameboid forms known to release a number of proinfl ammatory substances, may contribute to the neuroprotective effect of T cells. Supported by the grant no N401-1293-33 of the Ministry of Scientifi c Research and Information Technology in Poland.
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