Insulin-like growth factor 1 promotes cord blood T cell maturation and inhibits its spontaneous and phytohemagglutinin-induced apoptosis through different mechanisms

Functional immaturity of neonatal T cells is related to their immature phenotype, with the majority of neonatal T cells of naive (CD45RA(+)) T cells, The progression of T cells from naive cells to effector cells is dependent on the survival of Ag-specific T cells and their resistance to apoptosis, In this study, we showed for the first time that insulin-like growth factor 1 (IGF-1) converted cord blood CD45RA(+) T cells to CD45RO(+) T cells and inhibited cord blood T cell apoptosis, We found cord blood T cells stimulated with PHA would result in gradual loss of CD45RA and gain of CD45RO expression. IGF-1 further increased the loss of CD45RA and enhanced CD45RO expression in PRA-stimulated cord blood T cells. In addition, IGF-1 prevented cord blood T cells from spontaneous apoptosis through a mechanism other than Fas/FasL, In PHA-activated cord blood T cells, IGF-1 prevented both naive (CD45RA(+)) and memory/mature (CD45RO(+)) T cells from apoptosis, Moreover, cord blood T Cells cultured with IGF-1 and PHA had a higher resistance to anti-Fas-induced apoptosis as compared with PHA-activated cord blood T cells, IGF-1 also significantly inhibited PHA-induced Fas expression an cord blood T cells. These results demonstrate that IGF-1 promotes the maturation and maintains the survival of cord blood T cells, Its antiapoptotic effect in PHA-activated cord blood T cells may be mediated through the down-regulation of Fas expression.