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IL-6 receptor blockade corrects defects of XIAP-deficient regulatory T cells.

Abstract：

:X-linked lymphoproliferative syndrome type-2 (XLP-2) is a primary immunodeficiency disease attributed to XIAP mutation and is triggered by infection. Here, we show that mouse Xiap-/- regulatory T (Treg) cells and human XIAP-deficient Treg cells are defective in suppressive function. The Xiap-/- Treg cell defect is linked partly to decreased SOCS1 expression. XIAP binds SOCS1 and promotes SOCS1 stabilization. Foxp3 stability is reduced in Xiap-/- Treg cells. In addition, Xiap-/- Treg cells are prone to IFN-γ secretion. Transfer of wild-type Treg cells partly rescues infection-induced inflammation in Xiap-/- mice. Notably, inflammation-induced reprogramming of Xiap-/- Treg cells can be prevented by blockade of the IL-6 receptor (IL-6R), and a combination of anti-IL-6R and Xiap-/- Treg cells confers survival to inflammatory infection in Xiap-/- mice. Our results suggest that XLP-2 can be corrected by combination treatment with autologous iTreg (induced Treg) cells and anti-IL-6R antibody, bypassing the necessity to transduce Treg cells with XIAP.

journal_name

Nat Commun

journal_title

Nature communications

authors

Hsieh WC,Hsu TS,Chang YJ,Lai MZ

doi

10.1038/s41467-018-02862-4

subject

Has Abstract

pub_date

2018-01-31 00:00:00

pages

463

issue

1

issn

2041-1723

pii

10.1038/s41467-018-02862-4

journal_volume

9

pub_type

杂志文章

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