Blood 2012,
PMID: 23033269
Kleinsteuber, Katja; Heesch, Kerrin; Schattling, Stefanie; Sander-Juelch, Claudia; Mock, Ulrike; Riecken, Kristoffer; Fehse, Boris; Fleischer, Bernhard; Jacobsen, Marc
SOCS3 is a feedback regulator of cytokine signaling that affects T-cell polarization. Human tuberculosis is accompanied by increased SOCS3 expression in T cells, and this may influence susceptibility against Mycobacterium tuberculosis. Because the role of SOCS3 in human T-cell function is not well defined, we characterized cytokine expression and proliferation of human T cells with differential SOCS3 expression in the present study. We established a flow cytometry-based method for SOCS3 protein quantification and detected higher SOCS3 levels induced by M tuberculosis specific T-cell activation and a transient decrease of SOCS3 expression in the presence of mycobacteria-infected macrophages. Notably increased SOCS3 expression was detected in IL-17-expressing T-cell clones and in CD161(+) T helper type 17 cells ex vivo. Ectopic SOCS3 expression in primary CD4(+) T cells by lentiviral transduction induced increased IL-17 production but diminished proliferation and viability. Recombinant IL-7 inhibited SOCS3 expression and reduced IL-17-expressing T-cell proportions. We concluded that higher SOCS3 expression in human T cells favors T helper type 17 cells. Therefore, increased SOCS3 expression in human tuberculosis may reflect polarization toward IL-17-expressing T cells as well as T-cell exhaustion marked by reduced proliferation.
Diseases/Pathways annotated by Medline MESH: Tuberculosis
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Text Mining Data
interleukin-17 → SOCS3: "
SOCS3 promotes
interleukin-17 expression of human T cells
"
SOCS3 → IL-17: "
Ectopic SOCS3 expression in primary CD4 ( + ) T cells by lentiviral transduction induced increased IL-17 production but diminished proliferation and viability
"
SOCS3 ⊣ IL-7: "
Recombinant IL-7 inhibited SOCS3 expression and reduced IL-17 expressing T-cell proportions
"
Manually curated Databases
No curated data.