Collectively, this meta-analysis proved that IL-2 rs2069762, IL-4 rs2243250, IL-6 rs1800795, IL-8 rs4073, IL-10rs1800871 and IL-10rs1800896 polymorphisms may confer susceptibility to TB, especially for Asians.
Using in vitro and ex vivo cell culture systems, we show that human M(IL-10) anti-inflammatory macrophages, present in TB-associated microenvironment, produce high levels of HIV-1.
Our findings strongly indicate that IAV coinfection compromises the host's ability to control Mtb infection via the production of IL-10 which was rapidly induced upon viral infection.
Collectively, this meta-analysis proved that IL-6 rs1800795, IL-8 rs4073, IL-10rs1800871, IL-10rs1800872 and IL-10rs1800896 may confer susceptibility to TB.
Here, we show that pulmonary BCG prevents infection by using a repeated limiting-dose Mycobacterium tuberculosis challenge model and identify polyfunctional T-helper type 17 (T<sub>H</sub>17) cells, interleukin-10 and immunoglobulin A as correlates of local protective immunity.
Our data demonstrated that IL-2, IL-6, IL-10, and IFN-γ may be useful in the auxiliary diagnosis of tuberculosis and as biomarkers for distinguishing LTBI from TB.
Neutrophils can express cytokines that influence TB progression, and so we compared neutrophil and T-cell expression of the Th1 cytokines IFNγ and TNF, the Th2 cytokine IL-4, and regulatory cytokine IL-10 in M. tuberculosis-infected macaques to determine if neutrophil cytokine expression contributes to dysregulated immunity in TB.
To increase our understanding of immune response to M. tuberculosis infection, we conducted a cross-sectional study investigating M. tuberculosis infection status and comparing the release profiles of cytokines GM-CSF, IFN-γ, IL-1β, IL-10, IL-12 (p70), IL-2, IL-4, IL-5, IL-6, IL-8, TNF-α, in community controls (CCs) and healthy healthcare workers (HCWs) highly exposed to TB.
Multivariate analysis identified an IL-6/IL-10 co-expression-based principal component in tuberculosis patients that correlated with high pSTAT3 levels.
Moreover, we observed a positive correlation between the levels of IL-10 and the number of lipid-laden CD14<sup>+</sup> cells among the pleural cells in TB patients, demonstrating that FM differentiation occurs within the pleural environment.
Finally, we also measured the levels of IL-10 family cytokines in tuberculosis antigen (purified protein derivative, PPD) stimulated and unstimulated LN culture supernatants.
Multivariate analysis identified an IL-6/IL-10 co-expression-based principal component in tuberculosis patients that correlated with high pSTAT3 levels.
IL10 inhibits the function of Th1 type cells, and IL10 deficiency has been associated with an improved resistance against Mycobacterium tuberculosis infection in a mouse model.
This suggests that the IL-20 subfamily of cytokines, similar to IL-10 might play a potentially crucial role in the modulation of T cell responses in active TB disease.
The production of INF-γ but not IL-10 in the presence of purified protein, Rv0147, may be shifted to Th1 responses in MDR-TB patients and supports its potential as protein vaccine candidates against TB.
Interestingly, both HIV-TB and HD showed a pronounced production of IFN-γ in uTreg population, though no significant differences were observed for IL-10 and TGF-β production between uTreg and cTreg.
Diminished levels of ESAT-6/CFP-10-induced IL-10 and increased levels of TB-antigen and LPS-stimulated sCD163 were found in childhood with pulmonary TB.
Our findings from a study of naturally infected human population suggest that IFN-γ, TNF-α and IL-10 against rESAT-6/CFP-10 are markers for clinical TB but not for protective immunity.
Together, our data reveal that, despite the multiple immune sources of IL-10 during <i>M. tuberculosis</i> infection, activated effector T cells are the major source accounting for IL-10-induced TB susceptibility.