Open AccessInterleukin‐6: a new therapeutic target in systemic sclerosis?
Author(s) -
O'Reilly Steven,
Cant Rachel,
Ciechomska Marzena,
van Laar Jacob M
Publication year - 2013
Publication title -
clinical and translational immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.321
H-Index - 34
ISSN - 2050-0068
DOI - 10.1038/cti.2013.2
Subject(s) - immunology , rheumatoid arthritis , fibrosis , cytokine , autoimmune disease , disease , immune system , pathogenesis , medicine , inflammation , multiple sclerosis , receptor , biology , pathology , antibody
Interleukin‐6 (IL‐6) is a classic pro‐inflammatory cytokine critical in mounting an effective immune response. It is secreted by a wide array of cell types; however, its effector cells are more restricted, owing to the fact that very few cells, except lymphocytes and hepatocytes, express the functional membrane IL‐6 receptor thus reducing the number of IL‐6‐responsive cells. Trans‐signalling, the shedding of the membrane‐bound form of the IL‐6 receptor into the local microenvironment, greatly increases the range of cells that can respond. IL‐6 has been demonstrated to have a pivotal role in the pathogenesis of rheumatoid arthritis, Castleman's disease and Crohn's disease exemplified by the use of an anti‐IL‐6 biological therapy. However, IL‐6 is also associated with the autoimmune disease systemic sclerosis (SSc) and has been shown to be directly fibrotic. Elevated levels of IL‐6 are found in SSc patients and this correlates with skin thickness, suggesting a causal effect. This review focuses on the role of IL‐6 in SSc, a chronic autoimmune disease with fibrosis. In particular, we will examine the evidence base of the role of IL‐6 in fibrosis in this condition, especially the downstream effector pathways. We will then argue why molecular targeting of IL‐6 is a promising therapeutic target in this fibrosing disease.