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Constitutive STAT3 phosphorylation and IL-6/IL-10 co-expression are associated with impaired T-cell function in tuberculosis patients

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Cellular & Molecular Immunology 2019年第3期16卷 275-287页

作者： Kirstin Harling Ernest Adankwah Alptekin Güler Anthony Afum-Adjei Awuah Louis Adu-Amoah Ertan Mayatepek Ellis Owusu-Dabo norman nausch Marc Jacobsen Department of General Pediatrics Neonatologyand Pediatric CardiologyUniversity Children’s HospitalDuesseldorf 40225Germany Kumasi Centre for collaborative Research in Tropical Medicine(KCCR) KumasiGhana School of Public Health College of Health SciencesKwame Nkrumah University of Science and Technology(KNUST)KumasiGhana

T-cells critically contribute to protection against Mycobacterium tuberculosis infection,and impaired T-cell responses can lead to disease ***-inflammatory and immunosuppressive cytokines affect T-cells,and fine-tuned regulation of cytokine signaling via the Jak/STAT signaling pathways is crucial for appropriate T-cell *** STAT3 phosphorylation as a consequence of aberrant cytokine signaling has been described to occur in pathognomonic T-cell responses in inflammatory and autoimmune *** characterized blood samples from tuberculosis patients(n=28)and healthy contacts(n=28)from Ghana for ***-specific T-cell responses,constitutive cytokine production,and SOCS3 and pSTAT3 *** modulation of primary CD4+T-cells was performed to determine the effects of SOCS3 on T-cell functions.T-cells from tuberculosis patients expressed higher levels of IL-10 and IL-6 and lower levels of T helper type(TH)17 cytokines after ***-specific stimulation compared to healthy *** addition,tuberculosis patients had higher IL-10 and IL-6 levels in the supernatants of non-stimulated immune cells and plasma samples compared to healthy ***,aberrant cytokine expression was accompanied by high constitutive pSTAT3 levels and SOCS3 expression in *** analysis identified an IL-6/IL-10 co-expression-based principal component in tuberculosis patients that correlated with high pSTAT3 ***3 contributed to a regulatory component,and tuberculosis patients with high SOCS3 expression showed decreased TH1 cytokine expression and impaired IL-2-induced STAT5 ***3 over-expression in primary CD4+T-cells confirmed the SOCS3 inhibitory function on IL-2-induced STAT5 *** conclude that constitutive pSTAT3 and high SOCS3 expression are influential factors that indicate impaired T-cell functions in tuberculosis patients.

关键词： tuberculosis Interleukin-6 Interleukin-10 STAT3 SOCS3

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