The combination of IFN-γ, TNF-α, and IL-2R, and the combination of TNF-α, IL-2R, CXCL9, and CXCL10 showed the best performance for detecting active PTB (both 100% positivity) and LTBI (86.36% and 81.82% positivity, respectively).
In contrast to IFN-γ, the frequencies of CD4<sup>+</sup> or CD8<sup>+</sup> secreting TNF-α<sup>+</sup> cells were significantly high in PTB compared to LTBI.
However, the levels of IL-4 and TNF-α in the sera of patients from the PTB group did not show a significant correlation with those measured in the healthy donor group.
To examine the association of proinflammatory cytokines with pulmonary TB (PTB), we examined the plasma levels of type 1 (interferon [IFN]γ and tumor necrosis factor [TNF]α), type 17 (interleukin [IL]-17A and IL-17F), and other proinflammatory (IL-6, IL-12, and IL-1β) cytokines in individuals with PTB, latent TB (LTB), or healthy controls (HC).
247 HIV-TB (124 HIV-pulmonary TB, 123 HIV-extra pulmonary TB), 126 HIV positive individuals without tuberculosis and 129 healthy subjects (HS) were included to measure plasma levels of IFN-γ and TNF-α by sandwich ELISA and One way ANOVA statistical analysis was carried out among the groups.
Peripheral blood mononuclear cells from 42 healthy controls (HCs) and 42 pulmonary tuberculosis (PTB) patients were cultured with culture filtrate antigen (CFA) of Mtb with and without 1,25(OH)2D3 at 10(-7)M concentration for 72 h. The levels of IL-1α, IL-1β, TNF-α, TNF-β, IL-17 and IL-23 were estimated in the culture supernatants by ELISA.
To describe serum levels of the cytokines IL-10, TNF-α, and IFN-γ, as well as polymorphisms in the genes involved in their transcription, and their association with markers of the acute inflammatory response in patients with pulmonary tuberculosis.