Open Accessγδ T cell IFNγ production is directly subverted by Yersinia pseudotuberculosis outer protein YopJ in mice and humans
Author(s) -
Timothy Chu,
Camille Khairallah,
Jason Shieh,
Rhea Cho,
Zhijuan Qiu,
Yue Zhang,
Onur Eskiocak,
David G. Thanassi,
Mark H. Kaplan,
Semir Beyaz,
Vincent W. Yang,
James B. Bliska,
Brian S. Sheridan
Publication year - 2021
Publication title -
plos pathogens
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.719
H-Index - 206
eISSN - 1553-7374
pISSN - 1553-7366
DOI - 10.1371/journal.ppat.1010103
Subject(s) - yersinia pseudotuberculosis , microbiology and biotechnology , effector , biology , bacterial adhesin , yersinia , immune system , pathogen , t cell , virulence , gene , bacteria , immunology , genetics
Yersinia pseudotuberculosis is a foodborne pathogen that subverts immune function by translocation of Yersinia outer protein (Yop) effectors into host cells. As adaptive γδ T cells protect the intestinal mucosa from pathogen invasion, we assessed whether Y . pseudotuberculosis subverts these cells in mice and humans. Tracking Yop translocation revealed that the preferential delivery of Yop effectors directly into murine Vγ4 and human Vδ2 + T cells inhibited anti-microbial IFNγ production. Subversion was mediated by the adhesin YadA, injectisome component YopB, and translocated YopJ effector. A broad anti-pathogen gene signature and STAT4 phosphorylation levels were inhibited by translocated YopJ. Thus, Y . pseudotuberculosis attachment and translocation of YopJ directly into adaptive γδ T cells is a major mechanism of immune subversion in mice and humans. This study uncovered a conserved Y . pseudotuberculosis pathway that subverts adaptive γδ T cell function to promote pathogenicity.