Tim-3, a negative regulator of anti-tumor immunity

Anderson, Ana C.

doi:10.1016/j.coi.2011.12.005

Cited by 172 publications

(124 citation statements)

References 28 publications

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“…Several mechanisms of tumor cell immune evasion have been studied. One mechanism is the expression of immune checkpoint molecules on activated T cells infiltrating the tumor, including PD-1, cytotoxic T-lymphocyte-associated protein-4 and Tim-3 (24). Tim-3 is often co-expressed with PD-1 on exhausted T cells, which are T cells with a decreased ability to express cytotoxic cytokines, including IFN-γ and tumor necrosis factor-α, when they are continuously exposed to antigens (22).…”

Section: Discussionmentioning

confidence: 99%

Expression of the galectin-9-Tim-3 pathway in glioma tissues is associated with the clinical manifestations of glioma

Liu

Han

et al. 2016

Oncology Letters

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Abstract. Glioma is known to induce local and systemic immunosuppression, which inhibits antitumor T cell responses. The galectin-9-Tim-3-pathway negatively regulates T cell pathways in the tumor immunosuppressive environment. The present study assessed the expression of Tim-3 and galectin-9 in glioma patients, and evaluated the association between the expression of Tim-3 and galectin-9 with clinical characteristics. The present study identified that Tim-3 expression was significantly increased in peripheral blood T cells of glioma patients compared with those of healthy controls, and was additionally increased on tumor-infiltrating T cells. The expression of Tim-3 on tumor-infiltrating T cells was associated with the World Health Organization (WHO) grade of glioma, but negatively correlated with the Karnofsky Performance Status score of the glioma patients. Immunohistochemical analysis revealed that the expression of galectin-9 in tumor tissues was associated with Tim-3 expression on tumor-infiltrating T cells and the WHO grade of glioma. These findings suggest that the galectin-9-Tim-3 pathway may be critical in the immunoevasion of glioma and may be a potent target for immunotherapy in glioma patients.

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Section: Discussionmentioning

confidence: 99%

Expression of the galectin-9-Tim-3 pathway in glioma tissues is associated with the clinical manifestations of glioma

Liu

Han

et al. 2016

Oncology Letters

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“…The expression of Tim-3 on T cells in cancer may induce T cell exhaustion, and promote the expansion of immunosuppressive CD4CFoxP3C regulatory T (Treg) cells and CD11bCGr-1C myeloid suppressor cells (MDSC). 10 Recent reports also showed that TIM-3, as a surface molecule, is selectively expressed on leukemia stem cells (LSCs) in acute myeloid leukemia (AML), and as such it can be a good target in eradicating AML stem cells, leaving normal hematopietic stem cells intact. [11][12][13] In addition, Tim-3 has also been reported to up-regulate on tumor associated dendritic cells (TADC) and macrophages (TAM), and attenuate the antitumor effects of cancer vaccines 4 ( Fig.…”

Section: Introductionmentioning

confidence: 99%

Tim-3 and Tim-4 as the potential targets for antitumor therapy

Cheng

Ruan

2015

Human Vaccines & Immunotherapeutics

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“…Taken together, these results demonstrate that Tim-3 was expressed in the Th1 and synovial cells of patients with RA. In addition, Tim-3 overexpression may promote the activation and proliferation of tumor cells and macrophages (25)(26)(27). The present study also conducted a MTT assay to detect the effects of Tim-3 siRNA on the LPS-induced proliferation of FLS.…”

Section: Discussionmentioning

confidence: 99%

Effects of Tim-3 silencing on the viability of fibroblast-like synoviocytes and lipopolysaccharide-induced inflammatory reactions

Long

Chen

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. The objective of the present study was to investigate the effects of Tim-3 silencing on cell viability and lipopolysaccharide (LPS)-induced inflammatory reactions in fibroblast-like synoviocytes (FLS). T-cell immunoglobulin mucin domain molecule (Tim)-3 expression in FLS obtained from patients with rheumatoid arthritis (RA) and normal controls were detected by western blot analysis and reverse transcription-polymerase chain reaction (RT-PCR). Small interfering (si)RNA was transfected using Lipofectamine ® 2000 to decrease Tim-3 expression. Following transfection, FLS were stimulated by LPS. An MTT assay, RT-PCR and western blot analysis were performed to measure cell viability, Toll-like receptor 4 (TLR4) signaling pathway-related protein expression and inflammatory cytokine release, respectively. The results of the present study indicated that Tim-3 expression was increased in FLS from patients with RA compared with FLS from healthy controls. Transfection of Tim-3 siRNA significantly decreased Tim-3 expression in FLS from patients with RA. Notably, Tim-3 silencing decreased FLS cell viability. Following stimulation with LPS, cell viability and the expression of TLR4, myeloid differentiation protein gene 88 (MyD88) and nuclear factor-κB (NF-κB) p65 were enhanced in FLS. By contrast, Tim-3 silencing attenuated LPS-induced cell proliferation and the expression of TLR4, MyD88 and NF-κB p65. In addition, LPS significantly increased levels of cytokines in the supernatant, including tumor necrosis factor-α, interferon-γ and interleukin-6 (P<0.01). By contrast, Tim-3 silencing significantly decreased LPS-induced cytokine release (P<0.01). However, Tim-3 silencing did not affect TLR4, MyD88 and NF-κB p65 expression and the release of cytokines in cells that did not undergo treatment with LPS. Therefore, the results of the present study indicate that Tim-3 silencing decreases the viability of FLS in RA and attenuates the LPS-induced inflammatory reaction.

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Tim-3, a negative regulator of anti-tumor immunity

Cited by 172 publications

References 28 publications

Expression of the galectin-9-Tim-3 pathway in glioma tissues is associated with the clinical manifestations of glioma

Expression of the galectin-9-Tim-3 pathway in glioma tissues is associated with the clinical manifestations of glioma

Tim-3 and Tim-4 as the potential targets for antitumor therapy

Effects of Tim-3 silencing on the viability of fibroblast-like synoviocytes and lipopolysaccharide-induced inflammatory reactions

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