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Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with widespread inflammation, immune dysregulation, and is associated with the generation of destructive anti-DNA autoantibodies. We have shown previously the immune modulatory properties of pCons peptide in the induction of both CD4 +  and CD8 +  regulatory T cells which can in turn suppress development of the autoimmune disease in (NZB/NZW) F1 (BWF1) mice, an established model of lupus. In the present study, we add novel protein information and further demonstrate the molecular and cellular phenotypes of pCons-induced CD4 +  and CD8 +  T reg  subsets. Flow cytometry analyses revealed that pCons induced CD8 +  T reg  cells with the following cell surface molecules: CD25 high CD28 high and low  subsets (shown earlier), CD62L high , CD122 low , PD1 low , CTLA4 low , CCR7 low  and 41BB high . Quantitative real-time PCR (qRT-PCR) gene expression analyses revealed that pCons-induced CD8 +  T reg  cells downregulated the following several genes: Regulator of G protein signaling ( RGS2), RGS16, RGS17 ,  BAX, GPT2, PDE3b, GADD45β and  programmed cell death  1 (PD1).  Further, we confirmed the down regulation of these genes by Western blot analyses at the protein level. To our translational significance, we showed herein that pCons significantly increased the percentage of CD8 + FoxP3 +  T cells and further increased the mean fluorescence intensity (MFI) of FoxP3 when healthy peripheral blood mononuclear cells (PBMCs) are treated with pCons (10 μg/ml, for 24-48 hours). In addition, we found that pCons reduced apoptosis in CD4 +  and CD8 +  T cells and B220 +  B cells of BWF1 lupus mice. These data suggest that pCons stimulates cellular, immunological, and molecular changes in regulatory T cells which in turn protect against SLE autoimmunity.

Cellular and Molecular Phenotypes of pConsensus Peptide (pCons) Induced CD8+ and CD4+ Regulatory T Cells in Lupus