Tim‐3 expression on peripheral monocytes and <scp>CD3</scp>+<scp>CD16</scp>/<scp>CD56</scp>+natural killer‐like T cells in patients with chronic hepatitis B

Rong, Yihui; Wan, Zhihong; Song, Haihan; Li, Y.-L.; Zhu, Bing; Hong, Zhigang; Zhao, Yiwei; Liu, H.-L.; Zhang, A.-M.; Xiao, Long; Xin, Sun; You, Shaoli

doi:10.1111/tan.12278

Cited by 28 publications

(21 citation statements)

References 21 publications

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“…Tim-3 expression on monocytes is also positively associated with the level of ALT in patients with CHB, indicating its role in disease progression [49] . Concordantly, expression is increased on monocytes from patients with HCV infection and is positively correlated with IL-17 levels in CD4 + T cells, thus promoting Th17 cell accumulation.…”

Section: Tim-3 and Monocytes/macrophagesmentioning

confidence: 99%

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Role of Tim-3 in hepatitis B virus infection: An overview

Liu

Gao

Liang

et al. 2016

WJG

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Hepatitis B virus (HBV) infection has received increasing public attention. hBV is the prototypical member of hepadnaviruses, which naturally infect only humans and great apes and induce the acute and persistent chronic infection of hepatocytes. A large body of evidence has demonstrated that dysfunction of the host anti-viral immune response is responsible for persistent HBV replication, unresolved inflammation and disease progression. Many regulatory factors are involved in immune dysfunction. Among these, T cell immunoglobulin domain and mucin domain-3 (Tim-3), one of the immune checkpoint proteins, has attracted increasing attention due to its critical role in regulating both adaptive and innate immune cells. In chronic HBV infection, Tim-3 expression is elevated in many types of immune cells, such as T helper cells, cytotoxic T lymphocytes, dendritic cells, macrophages and natural killer cells. Tim-3 over-expression is often accompanied by impaired function of the abovementioned immunocytes, and Tim-3 inhibition can at least partially rescue impaired immune function and thus promote viral clearance. A better understanding of the regulatory role of Tim-3 in host immunity during HBV infection will shed new light on the mechanisms of hBV-related liver disease and suggest new therapeutic methods for intervention.

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Section: Tim-3 and Monocytes/macrophagesmentioning

confidence: 99%

“…NKT [49] . Above all, elevated Tim-3 expression is observed in innate immunocytes and exerts a suppressive effect on their function during HBV infection (Figure 1).…”

Section: Tim-3 and Nk/nktsmentioning

confidence: 99%

Role of Tim-3 in hepatitis B virus infection: An overview

Liu

Gao

Liang

et al. 2016

WJG

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“…Similar NK-like T cell subsets appear to be normal components of regional host defense in the gut. They may have auxiliary antitumor effect and have been associated with antiviral immunity in the setting of allergies and chronic hepatitis B disease (197–200). …”

Section: Nk-like T Cells In Young Persons With Chronic Diseases: a Camentioning

confidence: 99%

Functionally Diverse NK-Like T Cells Are Effectors and Predictors of Successful Aging

2016

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The fundamental challenge of aging and long-term survivorship is maintenance of functional independence and compression of morbidity despite a life history of disease. Inasmuch as immunity is a determinant of individual health and fitness, unraveling novel mechanisms of immune homeostasis in late life is of paramount interest. Comparative studies of young and old persons have documented age-related atrophy of the thymus, the contraction of diversity of the T cell receptor (TCR) repertoire, and the intrinsic inefficiency of classical TCR signaling in aged T cells. However, the elderly have highly heterogeneous health phenotypes. Studies of defined populations of persons aged 75 and older have led to the recognition of successful aging, a distinct physiologic construct characterized by high physical and cognitive functioning without measurable disability. Significantly, successful agers have a unique T cell repertoire; namely, the dominance of highly oligoclonal αβT cells expressing a diverse array of receptors normally expressed by NK cells. Despite their properties of cell senescence, these unusual NK-like T cells are functionally active effectors that do not require engagement of their clonotypic TCR. Thus, NK-like T cells represent a beneficial remodeling of the immune repertoire with advancing age, consistent with the concept of immune plasticity. Significantly, certain subsets are predictors of physical/cognitive performance among older adults. Further understanding of the roles of these NK-like T cells to host defense, and how they integrate with other physiologic domains of function are new frontiers for investigation in Aging Biology. Such pursuits will require a research paradigm shift from the usual young-versus-old comparison to the analysis of defined elderly populations. These endeavors may also pave way to age-appropriate, group-targeted immune interventions for the growing elderly population.

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“…Like PD-1, TIM-3 is expressed on IFN-γ-secreting CD4 + T-helper 1 cells (Th1), CTLs and NK cells [23,43]. Coexpression of TIM-3 and PD-1 on CTLs is a hallmark of T-cell exhaustion.…”

Section: Tim-3mentioning

confidence: 99%

Rationally Combining Anti-VEGF Therapy with Checkpoint Inhibitors in Hepatocellular Carcinoma

2016

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Hepatocellular carcinoma (HCC) is a fatal disease with rising incidence in the world. For advanced HCC, sorafenib, a multikinase inhibitor, is the only systemic therapy with proven survival benefits. Sorafenib is a pan-VEGF receptor inhibitor, and thus many studies have focused its antivascular effects. But VEGF also acts as an immunosuppressive molecule. VEGF can inhibit maturation of dendritic cells, promote immune suppressive cell infiltration and enhance immune checkpoint molecules expression. On the other hand, potent VEGF inhibition may increase tumor hypoxia, which could hinder antitumor immunity or immunotherapy. Thus, achieving synergy when combining anti-VEGF therapy with immunotherapy may require proper polarization of the tumor microenvironment by dose titration or combination with other immunomodulating agents.

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Tim‐3 expression on peripheral monocytes and CD3+CD16/CD56+natural killer‐like T cells in patients with chronic hepatitis B

Cited by 28 publications

References 21 publications

Role of Tim-3 in hepatitis B virus infection: An overview

Role of Tim-3 in hepatitis B virus infection: An overview

Functionally Diverse NK-Like T Cells Are Effectors and Predictors of Successful Aging

Rationally Combining Anti-VEGF Therapy with Checkpoint Inhibitors in Hepatocellular Carcinoma

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