IL-17 and IL-22: siblings, not twins

被引:204
作者
Eyerich, Stefanie [1 ,2 ,3 ]
Eyerich, Kilian [2 ,3 ,4 ]
Cavani, Andrea [4 ]
Schmidt-Weber, Carsten [1 ]
机构
[1] Imperial Coll London, Natl Heart & Lung Inst, Dept Allergy & Clin Immunol, London, England
[2] Tech Univ Munich, Div Environm Dermatol & Allergy, Helmholtz Ctr Munich Tech Univ Munich, Munich, Germany
[3] Tech Univ Munich, ZAUM Ctr Allergy & Environm, Munich, Germany
[4] IRCCS, Immunol Lab, Ist Dermopat Immacolata, Rome, Italy
关键词
COLLAGEN-INDUCED ARTHRITIS; GROWTH-FACTOR-BETA; T-HELPER-CELLS; ARYL-HYDROCARBON RECEPTOR; MUCOSAL HOST-DEFENSE; TH17; CELLS; GENE-EXPRESSION; INTERLEUKIN; 22; CUTTING EDGE; T-H-17;
D O I
10.1016/j.it.2010.06.004
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
T helper (Th) cell subsets secrete cytokines that regulate other immune cells. Interleukin (IL)-17 and IL-22 belong to a new class of cytokines with predominant effects on epithelial cells. Thus, these cytokines are key molecules in several disease processes. IL-17 and IL-22 are released by leukocytes such as Th and natural killer cell populations. Both IL-17 and IL-22 induce an innate immune response in epithelial cells, but their functional spectra are generally distinct. IL-17 induces an inflammatory tissue response and is involved in the pathogenesis of several autoimmune diseases, whereas IL-22 is protective/regenerative. This review juxtaposes IL-17 and IL-22 and describes overlaps and differences regarding their cellular sources, biochemical structure, signaling cascades in target cells, and function.
引用
收藏
页码:354 / 361
页数:8
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