After 24 hr ESAT-6 1 <i>μ</i>g/ml stimulation, the percentage of IL-1b-expressed hMDM was borderline lower in the active TB patients (<i>n</i> = 9) than in the LTBI cases (<i>n</i> = 10) (14.0 ± 11.2% vs. 31.6 ± 22.5%, <i>P</i> = 0.065).
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.
The F/B ratio was positively related to the detectable IL-1B in TB (R<sup>2</sup> = 0.97, P < 0.01) and to the IL-4 in LTBI (R<sup>2</sup> = 0.27, P < 0.05).
Impairment in TNF, IL-1β, and IL-17 production upon stimulation with mycobacterial antigens may contribute to the increased susceptibility to M. tuberculosis infection observed in HTLV-1 infected individuals.
Within the cohort of HIV-positive subjects, the expression profiles of 7 genes at baseline (FCGR1A, RAB24, TLR1, TLR4, MMP9, NLRC4, and IL1B) could accurately discriminate between active tuberculosis and both latent and no M. tuberculosis infection, largely independently of (in)eligibility for highly active antiretroviral therapy (HAART).
Interleukin-37 (IL-37), a novel member of the IL-1 family, plays fundamental immunosuppressive roles by broadly reducing both innate inflammation and acquired immunity, but whether it is involved in the pathogenesis of tuberculosis (TB) has not been clearly elucidated.
Following multivariate analyses adjusting for covariates IL6, interleukin 1β (IL1β), and interleukin 1Rα (IL1Rα) were associated with increased risk and IFNβ with decreased TB risk.
Our results with CLEC9A-knocked down cells and a CLEC9A-Fc fusion protein as blocking agents show that CLEC9A is involved in the activation of SYK and MAPK signaling in response to heat-killed M. tuberculosis H37Ra treatment, and it then promotes the production of CXCL8 and IL-1β in macrophages.
Production of IL-1β by innate immune cells following TLR and BCG stimulations correlated with differential TB recurrence outcomes in ART-treated patients and highlights differences in host response to TB.
We systematically searched published literatures on IL-1β gene and IL-6 gene polymorphisms and tuberculosis risk by the PubMed, Medline, Embase, Web of Science, Elsevier Science Direct and Cochrane Library databases, and identified outcome data from all articles.
These observations support a specific role for IL-1β and granulocytic inflammation as a driver of TB disease progression in humans, and suggest novel strategies for the prevention and treatment of tuberculosis.