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Pancreatic lymph node-derived CD4(+)CD25(+) Treg cells: highly potent regulators of diabetes that require TRANCE-RANK signals.

Abstract：

:Inflammation can activate self-reactive CD8(+) T cells and induce autoimmunity. Here we show in a CD8(+) T cell-mediated model of type 1 diabetes that CD4(+)CD25(+) Treg cells prevent beta cell destruction following localized inflammation in the islets of Langerhans. These Treg cells accumulate preferentially in the pancreatic lymph nodes and islets but not other lymph nodes or spleen. PLN-derived Treg cells are extremely potent; only 2 x 10(3) cells are needed to prevent diabetes development, and their capacity to regulate is dependent on TNF-related activation induced cytokine-receptor activator of NFkappaB signals. Indeed, blockade of this pathway results in decreased frequency of CD4(+)CD25(+) Treg cells in the PLN, resulting in intra-islet differentiation of CD8(+) T cells into CTLs and rapid progression to diabetes.

journal_name

Immunity

journal_title

Immunity

authors

Green EA,Choi Y,Flavell RA

doi

10.1016/s1074-7613(02)00279-0

keywords:

subject

Has Abstract

pub_date

2002-02-01 00:00:00

pages

183-91

issue

2

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(02)00279-0

journal_volume

16

pub_type

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