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The authors found that Salmonella Typhimurium infection augmented Tim-3 expression on intestinal lamina propria CD4(+) T cells and enhanced galectin-9 expression on F4/80(+) CD11b(+) macrophages.
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TIM-3 expression was predominantly localized to myeloid cells in both human and murine tumors
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Here, the authors demonstrate that Tim-3 inhibits macrophage phagocytosis of Listeria monocytogenes by inhibiting the nuclear erythroid 2-related factor 2 (Nrf2) signaling pathway and increases bacterial burden.
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Studied role of Tim-3 role's in T cell activation using a chronic disease model. Results showed a major function of Tim-3 is to enhance T cell activation during either acute or chronic viral infection, and that Tim-3 is not required for the development of T cell exhaustion.
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the data suggested that Tim-3 played a crucial role in the macrophage polarization and brain inflammation following intracerebral hemorrhage
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Tim-3 might contribute to successful pregnancy by restraining Th1 bias
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synergism in cell death by Caspase-1- and RipK3 resulted in restriction of PD-1 and TIM3 expression on primed CD8(+) T cells, which promoted the survival of activated CD8(+) T cells.
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these findings reveal a critical role for Tim-3-Gal-9 signaling-mediated immunoregulation by pNK cells in maternal-fetal immune tolerance and suggest that Tim-3 abundance on pNK cells is a potential biomarker for recurrent miscarriage diagnosis.
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Tim-3 and PD-1 pathways play critical roles in regulating CD8(+) T cell function and maintaining normal pregnancy.
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CB2R may have a crucial neuroprotective role following HI insult through the modulation of the inflammatory-related HIF-1alpha/TIM-3 signalling pathway in microglia
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Our results show that Tim-3 is a critical negative regulator of NLRP3 inflammasome and provides a potential target for intervention of diseases with uncontrolled inflammasome activation.
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demonstrated that both IL-10 and TGF-beta upregulated TIM-3 surface expression on dendritic cells via a common signaling pathway that involved sequential activation of c-Src and Bruton's tyrosine kinase
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Methylation level of the TIM-3 promoter gradually decreased after each round of T-cell polarization, and this decrease was inversely correlated with TIM-3 expression.
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in mice, TIM-3 is not essential for development of HDM-induced acute or chronic allergic airway inflammation, although it appears to be involved in reduced lymphocyte recruitment during HDM-induced chronic allergic airway inflammation.
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Authors found that a CD8(+) T-cell population with age-associated exhaustion was distinguishable by its expression of Tim-3.
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TIM4 binds TIM3 on the surface of polarized Th1 cells to induce Th1 cell apoptosis, which may contribute to the development of Th2-dominant immune disorders.
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decreases immunological rejection during composite tissue allotransplantation
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The Gal-9/Tim-3 signal is important for the regulation of decidua NK cells function, which is beneficial for the maintenance of a normal pregnancy.
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TIM-3 expression by NK cells and gamma/delta T cells is similar in the peripheral and decidual immune cells from pregnant mice.
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Tim-3 acts at a receptor-proximal point to enhance Lyn kinase-dependent signaling pathways that modulate both immediate-phase degranulation and late-phase cytokine production downstream of FcepsilonRI ligation.
