The novel interleukin-1 cytokine family members in inflammatory diseases

被引:45
作者
Hahn, Madelaine
Frey, Silke
Hueber, Axel J. [1 ,2 ]
机构
[1] Friedrich Alexander Univ Erlangen Nurnberg, Dept Internal Med 3, Univ Str 25a, D-90154 Erlangen, Germany
[2] Friedrich Alexander Univ Erlangen Nurnberg, Inst Clin Immunol, Univ Str 25a, Erlangen, Germany
关键词
inflammatory arthritis; inflammatory bowel disease; interleukin-1; family; neutrophil granulocytes; psoriasis; SYSTEMIC-LUPUS-ERYTHEMATOSUS; IL-36 RECEPTOR ANTAGONIST; RHEUMATOID-ARTHRITIS; BOWEL-DISEASE; EXPRESSION; PSORIASIS; PROTEIN; PROLIFERATION; NOMENCLATURE; IL-1F7B;
D O I
10.1097/BOR.0000000000000361
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of review This review provides an update on the new interleukin-1 (IL-1) cytokine family members in inflammatory diseases with focus on recent findings concerning the family members IL-36, IL-37, and IL-38 and their different expression patterns. Recent findings The IL-1 cytokines are known to be involved in many different inflammatory and autoimmune diseases. The latest IL-1 family members, IL-36, IL-37, and IL-38 have been shown to be differently regulated during course of disease. Studies of patients suffering from inflammatory diseases revealed that those cytokines are upregulated in the serum as well as in inflamed tissue. Both, epithelial cells and infiltrating peripheral mononuclear blood cells serve as source of the cytokines IL-36, IL-37, and IL-38 triggering different outcomes. These results could be confirmed in different mouse models and in-vitro and ex-vivo studies. Summary IL-36, IL-37, and IL-38 are involved in the pathogenesis of the inflammatory diseases psoriasis, rheumatoid arthritis, gout, systemic lupus erythematosus as well as Crohn's disease. Thereby IL-36 acts proinflammatory triggering further inflammatory mediators. In contrast, IL-37 and IL-38 are upregulated to counteract. Understanding the imbalance of the IL-1 family is crucial for future therapeutics.
引用
收藏
页码:208 / 213
页数:6
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