Targeting the IL-17/IFN-γ axis as a potential new clinical therapy for type 1 diabetes

被引：43

作者：

Marwaha, Ashish K. ^{[1
]}

Tan, Sara ^{[1
]}

Dutz, Jan P. ^{[1
]}

机构：

[1] Univ British Columbia, Fac Med, Child & Family Res Inst, Dept Dermatol & Skin Sci, Vancouver, BC V5Z 4E8, Canada

来源：

CLINICAL IMMUNOLOGY | 2014年 / 154卷 / 01期

关键词：

Ustekinumab; Stelara; Type; 1; diabetes; IL-17; IFN-gamma; Clinical trial; REGULATORY T-CELLS; TH17; CELLS; IFN-GAMMA; DOUBLE-BLIND; IL-17; CYTOKINE; MICE; INFLAMMATION; INHIBITION; INDUCTION;

D O I：

10.1016/j.clim.2014.06.006

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Type 1 diabetes (T1D) results from the autoimmune destruction of insulin-producing pancreatic beta cells. There is now mounting evidence that pro-inflammatory pathways, which are mediated by T cells that secrete IL-17 and IFN-gamma, play a critical role in the loss of beta cells. These data suggest that blockade of T cells that secrete IL-17 and IFN-gamma may halt or reverse disease in subjects with recent-onset T1D. Agents to facilitate this approach are currently in clinical use. Ustekinunnab, a humanized monoclonal antibody that targets the shared p40 subunit of IL-12 and IL-23, has been used for the treatment of psoriasis, an indication for which it has proven to be safe and effective. In this review, we summarize the evidence that supports a combined pathogenic role of IL-17 and IFN-gamma in the development of T1D, with the aim of providing a rationale for testing agents such as ustekinumab for the treatment of T1D. (C) 2014 Published by Elsevier Inc.

引用

页码：84 / 89

页数：6