We showed that HIV infection significantly reduced the proportion of Th2 (interleukin 4 [IL-4]/IL-5/IL-13) producing <i>M. tuberculosis</i>-specific CD4 T cells and IL-2-producing <i>M. tuberculosis</i>-specific CD4 and CD8 T cells in individuals with LTBI or PTB (<i>P < </i>0.05).
A strategy is described for continuous monitoring of multiple latent tuberculosis infection (LTBI) biomarkers, specifically of interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α) and interleukin-2 (IL-2).
Diagnostic performance of GM-CSF and IL-2 in response to long-term specific-antigen cell stimulation in patients with active and latent tuberculosis infection.
The proposed ECL-sensing platform is simple, sensitive, accurate, reliable, and specific to the detection of rare IFN-γ and IL-2 in human serum and provides a valuable protocol for facilitating fast and precise diagnosis of LTBI.
Our data reveal that individuals with LTB and coexistent <i>S. stercoralis</i> infection have significantly lower levels of systemic and TB antigen-stimulated type 1 (gamma interferon [IFN-γ], tumor necrosis factor alpha [TNF-α], and interleukin-2 [IL-2]) and type 17 (IL-17A and/or IL-17F) cytokines and significantly higher levels of systemic but not TB antigen-stimulated type 2 (IL-4 and IL-5) and regulatory (transforming growth factor beta [TGF-β]) cytokines.
This study confirms IL-2 induced by PE35 and PPE68 as a sensitive and specific biomarker and highlights IL-2 as new promising adjunct markers for discriminating of LTBI and active TB disease.
All M. tuberculosis-specific CD4+ subsets, with the exception ofIL-2-only cells, switched from central to effector memory phenotype in active tuberculosis vs latent tuberculosis infection, accompanied by a reduction in IL-7 receptor α (CD127) expression.