2012年5月1日 · Thus, Tim3/Gal9, via IL-1β and downstream TNF production lead to apoptosis and restriction of intracellular Mtb growth. We propose that Tim3/Gal9 interaction acts as a bidirectional molecular rheostat that activates pathways to clear intracellular pathogens in innate immune cells while fine-tuning termination of TH1 responses to prevent ...

2010年10月10日 · These data indicate that Tim3–Gal9 interaction leads to killing of Mtb independently of IFN-γ receptor signaling and iNOS production and strongly suggest that Tim3 activates a novel antibacterial pathway in Mtb -infected macrophages.

4 天之前 · For example, in Mtb infection TIM3 could mediate activation against galectin-9-expressing macrophages 51. Thus, further studies are needed to determine its role in the context of vaccination.

2016年3月11日 · Given the important role of TIM3 in mediating T cell exhaustion during chronic viral infections, we determined whether TIM3 regulates T cell function during tuberculosis. We show that CD4 + and CD8 + T cells become functionally exhausted during M. …

2022年1月25日 · In line with the animal studies, elevated TIM3 expression leads to decreased IFNγ production of CD8 + T cells in patients with active/severe Mtb infection, which can be restored by TIM3-blocking interventions (55).

Here, we reported an intriguing case of Mycobacterium tuberculosis (Mtb) infection that was characterized by persistent overexpression of TIM3 on circulating T cells and ongoing kidney tubulointerstitial inflammation for a period of 12 months.

We found that in Mtb infected Mϕ, Tim3 activates a program of antimicrobial immunity that involves the initial secretion of IL-1β followed by IL-1β mediated recruitment of other antimicrobial effectors including IL-6, TNF, MIP1α, MIP1β, and G-CSF.

T-cell immune responses modulated by T-cell immunoglobulin and mucin domain-containing molecule 3 (Tim-3) during Mycobacterium tuberculosis (Mtb) infection in humans remain poorly understood. Here, we found that active TB patients exhibited increases in numbers of Tim-3-expressing CD4 (+) and CD8 (+) …

The ability of pathogenic Mycobacterium tuberculosis (Mtb) to adapt to the hostile intracellu-lar environment of the macrophage has been in-strumental to its success as a pathogen. Host re-sistance against Mtb relies on TH1-mediated immunity (Flynn and Chan, 2001).

Tim-3 has gained prominence as a potential candidate for cancer immunotherapy, where it has been shown that in vivo blockade of Tim-3 with other check-point inhibitors enhances anti-tumor immunity and suppresses tumor growth in several preclinical tumor models.