signature=c5e7edd37cd6eb454d292f1e5c659469,Distinct gene signature revealed in white blood cells, CD...

摘要：

Tolerizing polygenically predisposed to -like disease (NZB/NZW F1 females) with a mimicking anti-DNA IgG sequences containing MHC class I and class II T cell determinants (pConsensus, pCons) results in protection from full-blown disease attributable in part to the induction of (+)CD25(+)+ and CD8(+)+ regulatory T cells. We compared 45 000 genes in total white blood cells (WBC), (+) T cells, and CD8(+) T cells from splenocytes of (NZBxNZW) F1 -prone tolerized with pCons vs untreated nave and found two-fold or greater differential expression for 448 WBC, 174 CD4, and 60 CD8 genes. We identified differentially expressed genes that played roles in the and . Using real-time , we validated differential expression of selected genes (IFI202B, , , -53, and IFNar1) in the CD8(+)T cell microarray and determined expression of selected highly upregulated genes in different immune cell subsets. We also determined Smads expression in different immune cell subsets, including (+) T cells and CD8(+) T cells, to detect the effects of TGF-beta, known to be the major cytokine that accounts for the suppressive capacity of CD8(+) Treg in this system. Silencing of anti-apoptotic gene or interferon genes (IFI202b and IFNar1 in combination) in CD8(+) T cells from tolerized did not affect the expression of the other selected genes. However, silencing of reduced expression of , and -all of which are involved in the suppressive capacity of CD8(+) Treg in this model.

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