Nat Immunol 2007,
PMID: 17581537
Zhou, Liang; Ivanov, Ivaylo I; Spolski, Rosanne; Min, Roy; Shenderov, Kevin; Egawa, Takeshi; Levy, David E; Leonard, Warren J; Littman, Dan R
T helper cells that produce interleukin 17 (IL-17; 'T(H)-17 cells') are a distinct subset of proinflammatory cells whose in vivo function requires IL-23 but whose in vitro differentiation requires only IL-6 and transforming growth factor-beta (TGF-beta). We demonstrate here that IL-6 induced expression of IL-21 that amplified an autocrine loop to induce more IL-21 and IL-23 receptor in naive CD4(+) T cells. Both IL-21 and IL-23, along with TGF-beta, induced IL-17 expression independently of IL-6. The effects of IL-6 and IL-21 depended on STAT3, a transcription factor required for the differentiation of T(H)-17 cells in vivo. IL-21 and IL-23 induced the orphan nuclear receptor RORgammat, which in synergy with STAT3 promoted IL-17 expression. IL-6 therefore orchestrates a series of 'downstream' cytokine-dependent signaling pathways that, in concert with TGF-beta, amplify RORgammat-dependent differentiation of T(H)-17 cells.
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Text Mining Data
transforming growth factor-beta → IL-23: "
T helper cells that produce interleukin 17 ( IL-17 ; ` T ( H ) -17 cells ' ) are a distinct subset of proinflammatory cells whose in vivo function requires
IL-23 but whose in vitro differentiation
requires only IL-6 and
transforming growth factor-beta ( TGF-beta )
"
IL-23 → IL-6: "
T helper cells that produce interleukin 17 ( IL-17 ; ` T ( H ) -17 cells ' ) are a distinct subset of proinflammatory cells whose in vivo function requires IL-23 but whose in vitro differentiation requires only IL-6 and transforming growth factor-beta ( TGF-beta )
"
IL-21 → IL-6: "
We demonstrate here that IL-6 induced expression of IL-21 that amplified an autocrine loop to induce more IL-21 and IL-23 receptor in naive CD4 ( + ) T cells
"
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