Moreover, to enhance vaccine immunogenicity, two toll-like receptors 4 (TLR4) agonists, resuscitation-promoting factors of Mycobacterium tuberculosis (RpfE and RpfB), were employed as the built-in adjuvants.
Polymorphisms in TLR4 and TNFA and Risk of Mycobacterium tuberculosis Infection and Development of Active Disease in Contacts of Tuberculosis Cases in Brazil: A Prospective Cohort Study.
Of note, network analysis comparing TB-associated host genes identified in the current HIV-negative TB cohort to TB-associated genes identified in our previously published Ethiopian HIV-positive TB cohort, revealed an over-representation of pattern recognition receptors including TLR2 and TLR4 in the HIV-positive cohort which was not seen in the HIV-negative cohort.
Elucidation of the immune mechanisms associated with tuberculosis (TB) development may help to control <i>M. tuberculosis</i> spread<i>.</i>OBJECTIVE: To investigate the role of TLR2, TLR4 and TLR9 in hindered in vitro microbicidal activity and increase T<sub>reg</sub> number during LTBI.
Some limited investigations approved the roles of TLR4 in induction of apoptosis in macrophages during tuberculosis (TB) and attenuation of immune responses in some situations.
Thus we studied the phagocytosis potential and expression of toll like receptors (TLR1, TLR2 and TLR4) and Fcγ receptors (CD64 and CD32) by human neutrophils following infection with Mycobacterium tuberculosis strains.
Monocyte-derived macrophages from healthy Filipinos, Chinese and non-Hispanic White study participants (approximately 45 individuals/group) were challenged with M. tuberculosis whole cell lysates of clinical strains Beijing HN878 (lineage 2), Manila T31 (lineage 1), CDC1551 (lineage 4), the reference strain H37Rv (lineage 4), as well as with Toll-like receptor 2 agonist lipoteichoic acid (TLR2/LTA) and TLR4 agonist lipopolysaccharide (TLR4/LPS).
Furthermore, the levels of TLR2, TLR4 and IFN-γ mRNA expression were marked increased in the tuberculous PE when compared with the correspondent serum.
Here, we sought to determine the role of B cells in the induction of T-helper 1 (T<sub>H</sub> 1) CD4<sup>+</sup> T cells upon vaccination with a tuberculosis (TB) antigen combined with a TLR4 agonist.
In conclusion, our data suggest that TLR4 (D299G and T399I) and TNF (-308G/A) genetic polymorphisms may influence the risk of developing tuberculosis after exposure to Mycobacterium.
By contrast, RSTR was associated with SNPs in NOD2, SLC6A3 and TLR4 (nominal P < 0.05); these genes were not associated with TB, suggesting distinct genetic influences.
TLR2, TLR4, and VDR polymorphisms were previously associated with tuberculosis (TB) and were here investigated as candidates for pulmonary TB (PTB) susceptibility in a Moroccan population group.
Furthermore, EREG expression was induced in monocytes and peripheral blood mononuclear cells stimulated with M. tuberculosis as well as TLR4 and TLR2/1/6 ligands.