Cutting Edge: IL-23 Receptor GFP Reporter Mice Reveal Distinct Populations of IL-17-Producing Cells

被引：309

作者：

Awasthi, Amit ^{[1
]}

Riol-Blanco, Lorena ^{[1
]}

Jaeger, Anneli ^{[2
]}

Korn, Thomas ^{[3
]}

Pot, Caroline ^{[2
]}

Galileos, George ^{[1
]}

Bettelli, Estelle ^{[2
]}

Kuchroo, Vijay K. ^{[2
]}

Oukka, Mohamed ^{[1
]}

机构：

[1] Harvard Univ, Sch Med, Brigham & Womens Hosp, Ctr Neurol Dis, Cambridge, MA 02139 USA

[2] Harvard Univ, Sch Med, Brigham & Womens Hosp, Ctr Neurol Dis, Boston, MA 02115 USA

[3] Tech Univ Munich, Dept Neurol, Munich, Germany

来源：

JOURNAL OF IMMUNOLOGY | 2009年 / 182卷 / 10期

基金：

美国国家卫生研究院; 瑞士国家科学基金会;

关键词：

T-CELLS; INFLAMMATION; DIFFERENTIATION; ASSOCIATION; CYTOKINE; IL23R; BETA;

D O I：

10.4049/jimmunol.0900732

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

IL-23, an IL-12 family member, has been implicated in the development of Th17 cells and the progression of autoimmune diseases. However, due to the lack of availability of sensitive Ab reagents specific for the IL-23 receptor (IL-23R), it has been difficult to characterize the cell types that express the IL-23R and are responsive to IL-23 in vivo. To address the role of IL-23 in vivo, we have generated a novel "knock-in" mouse in which we have replaced the intracellular domain of the IL-23R with the GFP. We show that in addition to Th17 cells, a subset of myeloid cells express IL-23R and respond to IL-23 by producing IL-17 and IL-22. Our studies further demonstrate that IL-23R expression is crucial for generation of encephalitogenic Th17 cells, but its expression on the innate immune system is dispensible in the development of experimental autoimmune encephalomyelitis. The Journal of Immunology, 2009, 182: 5904-5908.

引用

页码：5904 / 5908

页数：5

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