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Chitinase 3-like-1 deficient donor splenocytes accentuated the pathogenesis of acute graft-versus-host diseases through regulating T cell expansion and type I inflammation.

Abstract：

:Acute graft-versus-host disease (aGVHD) is a major complication following transplantation, limiting the success of this therapy. Chitinase 3-like-1 (CHI3L1), a member of the glycosyl hydrolase 18 family, plays a critical role in bacterial infections, allergic disease and a variety of malignancies. Here, we investigated whether CHI3L1 could affect the pathogenesis of aGVHD in a mouse allo-HCT model. In this study, we show that CHI3L1 deficiency in donor T cells increased the severity of aGVHD through enhancing systemic and local inflammation. In addition, we found that aGVHD induced by CHI3L1-knockout (CHI3L1-KO) donors resulted in massive expansion of donor CD3+ T cells, release of Th1-related cytokines and chemokines, and significant inhibition of CD4+CD25+Foxp3+ regulatory T cells (Tregs) without changing the suppressive ability of donor Tregs remarkably. Expression of PERK1/2 and PAkt increased both in the skin and intestine from CHI3L1-KO splenocytes-treated aGVHD mice. Moreover, at mRNA and protein levels, we defined several molecules that may account for the enhanced ability of CHI3L1-KO splenocytes to migrate into target organs and produce Th1-related cytokines and chemokines, such as CXCL9, CXCL11, IFN-γ and TNF-α. Therefore, these results imply that CHI3L1 levels in donor cells may be related to the risk of aGVHD and targeting CHI3L1 may be a promising clinical strategy to control aGVHD.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Li Z,Gu J,Liu J,Zhu Q,Lu H,Lu Y,Rao J,Lu L,Wang X

doi

10.1016/j.intimp.2017.03.010

subject

Has Abstract

pub_date

2017-05-01 00:00:00

pages

201-209

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(17)30100-5

journal_volume

46

pub_type

杂志文章

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