Abstract
The cAMP response element (CRE) modulator (CREM)α binds to promoters of genes with CREs and regulates transcription via a chromatin-dependent mechanism. CREMα is important for the T cell pathophysiology of SLE by suppression of IL-2 and CD3ζ but enhancement of IL-17 transcription. Juvenile idiopathic arthritis (JIA) is an autoimmune disease of unknown origin. Th17 cells have a pathogenic role in arthritis and are not controlled by local FoxP3+ regulatory T cells (Tregs). Pathogenic T cells in the inflamed joints of JIA patients have enhanced expression of IL-17, IFN-γ and CD161. CD161+ CD4+ cells also contain FoxP3+ cells that produce proinflammatory cytokines. A higher frequency of CD161 Tregs appears to associate with more severe disease in JIA, a fact which might contribute to the failure by Treg to suppress ongoing inflammation.
Highlights
The cAMP response element (CRE) modulator (CREM)a binds to promoters of genes with CREs and regulates transcription via a chromatin-dependent mechanism
PBMCS from healthy donors were incubated in the presence of synovial fluid from Juvenile idiopathic arthritis (JIA) patients
Enhanced expression of CREM was induced after ex vivo culture of peripheral blood mononuclear cells (PBMCs) from healthy donors with synovial fluid from JIA patients
Summary
The cAMP response element (CRE) modulator (CREM)a binds to promoters of genes with CREs and regulates transcription via a chromatin-dependent mechanism. CREMa is important for the T cell pathophysiology of SLE by suppression of IL-2 and CD3ζ but enhancement of IL-17 transcription. Juvenile idiopathic arthritis (JIA) is an autoimmune disease of unknown origin. Th17 cells have a pathogenic role in arthritis and are not controlled by local FoxP3+ regulatory T cells (Tregs). Pathogenic T cells in the inflamed joints of JIA patients have enhanced expression of IL-17, IFN-g and CD161. CD161+ CD4+ cells contain FoxP3+ cells that produce proinflammatory cytokines. A higher frequency of CD161 Tregs appears to associate with more severe disease in JIA, a fact which might contribute to the failure by Treg to suppress ongoing inflammation
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