title: Targeting IL-17 in autoimmunity and inflammation.
abstract: The discovery of two distinct subsets of helper T cells, IFN-γ-producing Th1 cells and IL-4-producing Th2 cells, about three decades ago enabled us to understand the immunopathology of cell-mediated and allergic inflammatory diseases in humans. The observation that T cell-mediated experimental autoimmune diseases can be induced in mice lacking Th1 and Th2 cell responses prompted many immunologists to hypothesize that there might be additional subsets in helper T cell population which mediate autoimmunity in the absence of Th1 and Th2 cells. Consequently, multiple independent research groups identified IL-17-expressing RORγt+CD4+T cell population as a distinct subset of helper T cells which promotes autoimmune tissue inflammation. Subsequent studies have revealed that innate immune cells, including γδ T cells, NKT cells and innate lymphoid cells, also produce type 17 cytokines and contribute to tissue inflammation. In this review, we discuss our current understanding on the biology of IL-17 and the therapeutic potential of targeting IL-17 for the treatment of immune disorders in humans.
authors: Laboratory of Immune Regulation, Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, 08826, Republic of Korea.|BK21 Plus Program, College of Pharmacy, Seoul National University, Seoul, 08826, Republic of Korea.
authors: Byung-Seok
authors: BS
authors: Kim
authors: Laboratory of Immune Regulation, Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, 08826, Republic of Korea.
authors: Young-Jun
authors: YJ
authors: Park
authors: Laboratory of Immune Regulation, Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, 08826, Republic of Korea. yeonseok@snu.ac.kr.|BK21 Plus Program, College of Pharmacy, Seoul National University, Seoul, 08826, Republic of Korea. yeonseok@snu.ac.kr.
authors: Yeonseok
authors: Y
authors: Chung
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000627:therapeutic use*; D001327:Autoimmune Diseases / Q000188:drug therapy* / Q000276:immunology; D015551:Autoimmunity / Q000187:drug effects; D002454:Cell Differentiation / Q000187:drug effects / Q000276:immunology; D002986:Clinical Trials as Topic; D006801:Humans; D007249:Inflammation / Q000188:drug therapy* / Q000276:immunology; D020381:Interleukin-17 / Q000037:antagonists & inhibitors* / Q000276:immunology; D053722:Receptors, Interleukin-17 / Q000037:antagonists & inhibitors / Q000276:immunology; D015398:Signal Transduction; D058504:Th17 Cells / Q000166:cytology / Q000276:immunology*
chemical_list: D000911:Antibodies, Monoclonal; D020381:Interleukin-17; D053722:Receptors, Interleukin-17
keywords: Anti-IL-17; Autoimmunity; IL-17; RORγt; Th17 cell