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. 2018 May 31;77(9):1362–1371. doi: 10.1136/annrheumdis-2018-213031

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Potential mechanisms of interaction between IL-6 and TGFβ leading to fibrosis in SSc. (1) Inflammatory macrophage-produced IL-6 enhances fibrogenic macrophage function (potential TCZ target). (2) IL-6 induces TGFβ production and enhances its signalling in fibroblasts (potential TCZ target). (3) TGFβ enhances IL-6 production by fibroblasts. (4) IL-6 directly activates fibroblasts to produce profibrotic proteins such as Col1 (potential TCZ target). (5) TGFβ directly induces fibroblast differentiation into myofibroblasts. (6) Intracellularly, IL-6 classic signalling and TGFβ alternative signalling converge towards the activation of STAT3 (STAT3 → P-STAT3) resulting in aberrant expression of STAT3-dependent genes. αSMA, alpha-smooth muscle actin; Col1, collagen alpha 1; CTGF, connective tissue growth factor; ECM, extracellular matrix; GF, growth factor; IL-6, interleukin-6; JAK, Janus-activated kinase; JNK, Jun N-terminal kinase; P-STAT, phosphorylated STAT; STAT, signal transducer and activator of transcription; TGFβ, transforming growth factor beta; TGFβR, transforming growth factor beta receptor; TYK, tyrosine kinase.