Targeted deletion of c-Met in thymic epithelial cells leads to an autoimmune phenotype.

Abstract:

:Hepatocyte growth factor (HGF) and its receptor c-Met signaling have been implicated in regulating various types of cells including epithelial cells. We have previously reported that c-Met is expressed by thymic epithelial cells (TECs), and that in vivo administration of hybrid cytokines containing IL-7 and the beta- or alpha-chain of HGF significantly increase the number of TECs. In order to study the role of c-Met signaling in TECs, we generated conditional knockout (cKO) mice in which c-Met was specifically deleted in TECs using a Foxn1-Cre transgene. We show here that c-Met deficiency in TECs results in age-progressive reduction in TEC number and reduced number of regulatory T cells. Consequently, c-Met TEC cKO mice displayed an autoimmune phenotype. Thus, c-Met signaling in TECs is important for the maintenance of TECs and immune self-tolerance.

journal_name

Immunol Cell Biol

authors

Su M,Hu R,Song Y,Liu Y,Lai L

doi

10.1111/imcb.1026

subject

Has Abstract

pub_date

2018-02-01 00:00:00

pages

229-235

issue

2

eissn

0818-9641

issn

1440-1711

journal_volume

96

pub_type

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