Abstract
T helper type 17 (Th17) cells and pTreg cells, which share a common precursor cell (the naïve CD4 T cell), require a common tumor growth factor (TGF)-β signal for initial differentiation. However, terminally differentiated cells fulfill opposite functions: Th17 cells cause autoimmunity and inflammation, whereas Treg cells inhibit these phenomena and maintain immune homeostasis. Thus, unraveling the mechanisms that affect the Th17/Treg cell balance is critical if we are to better understand autoimmunity and tolerance. Recent studies have identified many factors that influence this balance; these factors range from signaling pathways triggered by T cell receptors, costimulatory receptors, and cytokines, to various metabolic pathways and the intestinal microbiota. This review article summarizes recent advances in our understanding of the Th17/Treg balance and its implications with respect to autoimmune disease.
Highlights
The immune system provides essential protection against pathogenic microorganisms; it may attack self tissue
Naïve CD4 T cells are activated upon binding of the T cell receptor (TCR) and a costimulatory receptor (CD28) to the peptide–major histocompatibility complex (MHC) complex and a costimulatory molecule (B7.1 or B7.2), respectively; the latter are expressed/presented by antigen-presenting cells (APCs)
Since many autoimmune diseases are driven by Th17 cells and suppressed by Treg cells, the balance between these cell types is critically important for pathogenesis, prognosis, and therapy
Summary
The immune system provides essential protection against pathogenic microorganisms; it may attack self tissue. Treg cells produce anti-inflammatory cytokines IL-10 and TGF-β, suppress activity of a variety of immune cells, and thereby inhibit immune responses. These two cell types play opposite roles during inflammatory and immune responses [6]. STAT3 is activated upon stimulation by TCR/costimulatory signals, together with TGF-β and IL-6 [3,4,5]; STAT3 induces expression of transcription factor RAR-related orphan receptor (ROR)γt, which derives cells toward the Th17 subset [7]. Stimulation of naïve CD4 T cells with TGF-β induces SMAD2 and SMAD3, which in turn activate transcription factor Foxp; this drives cells toward the pTreg lineage [8]. I explain what we know about these factors, their role(s) in regulating the Th17/Treg balance, and the implications for development of autoimmunity
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