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PD‐1‐expressing MAIT cells from patients with tuberculosis exhibit elevated production of CXCL13
Author(s) -
Jiang Jing,
Cao Zhihong,
Qu Jiuxin,
Liu Houming,
Han Hongxing,
Cheng Xiaoxing
Publication year - 2020
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12858
Subject(s) - cxcl13 , flow cytometry , tuberculosis , cxcr5 , transcriptome , immunology , peripheral blood mononuclear cell , phenotype , biology , medicine , antibody , gene , gene expression , pathology , inflammation , b cell , in vitro , biochemistry , chemokine , germinal center , chemokine receptor
To understand functional role of PD‐1‐expressing MAIT cells during tuberculosis infection in humans, sorted PD‐1 + and PD‐1 − MAIT cells from pleural effusions of patients with pleural tuberculosis were subjected to transcriptome sequencing. PD‐1‐expressing MAIT cells were analysed by flow cytometry and their phenotypic and functional features were investigated. Transcriptome sequencing identified 144 genes that were differentially expressed between PD‐1 + and PD‐1 − MAIT cells from tuberculous pleural effusions and CXCL13 was the gene with highest fold difference. The level of PD‐1‐expressing MAIT cells was associated with extent of TB infection in humans. PD‐1‐expressing MAIT cells had increased production of CXCL13 and IL‐21 as determined by flow cytometry. PD‐1 high CXCR5 − MAIT cells were significantly expanded in pleural effusions from patients with pleural tuberculosis as compared with those from peripheral blood of both patients with tuberculosis and healthy controls. Although PD‐1 high CXCR5 − MAIT cells from tuberculous pleural effusions had reduced IFN‐γ level and increased expression of Tim‐3 and GITR, they showed activated phenotype and had higher glucose uptake and lipid content. It is concluded that PD‐1‐expressing MAIT cells had reduced IFN‐γ level but increased production of both CXCL13 and IL‐21.