β cells are responsible for CXCR3-mediated T-cell infiltration in insulitis

被引：252

作者：

Frigerio, S

Junt, T

Lu, B

Gerard, C

Zumsteg, U

Holländer, GA

Piali, L

机构：

[1] Res Dept, Basel, Switzerland

[2] Dept Clin Biol Sci, Basel, Switzerland

[3] Univ Childrens Hosp, Basel, Switzerland

[4] Univ Zurich, Inst Expt Immunol, CH-8006 Zurich, Switzerland

[5] Harvard Univ, Sch Med, Boston, MA 02115 USA

[6] Childrens Hosp, Perlmutter Lab, Boston, MA 02115 USA

来源：

NATURE MEDICINE | 2002年 / 8卷 / 12期

关键词：

D O I：

10.1038/nm792

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

T cell-mediated loss of insulin-secreting betacells in the islets of Langerhans is the hallmark of type 1 diabetes. The molecular basis for the directed migration of autoreactive T cells leading to insulitis is presently unknown. Here we demonstrate that in response to inflammation, betacells secrete the chemokines CXC ligand 10 and CXC ligand 9, which specifically attract T-effector cells via the CXC chemokine receptor 3. In mice deficient for this receptor, the onset of type 1 diabetes is substantially delayed. Thus, in the absence of known etiological agents, CXC receptor 3 represents a novel target for therapeutic interference early in type 1 diabetes.

引用

收藏

页码：1414 / 1420

页数：7

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