Mucosal-Associated Invariant T cell in liver diseases

Zhang, Yujue; Kong, Deyan; Wang, Hua

doi:10.7150/ijbs.39016

Cited by 18 publications

(24 citation statements)

References 92 publications

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“…The results showed that plasma levels of IL-12 and IL-18 were increased obviously in HBV-related liver failure. Zhang et al[ 35 ] concluded that, in parallel to the reduction of MAIT cells, the increase in IL-12 and IL-18 may contribute to MAIT cell activation, loss or death. We inferred that depletion of circulating MAIT cells might be caused by stimulation by IL-12 and IL-18 in HBV-related liver failure.…”

Section: Discussionmentioning

confidence: 99%

Mucosal-associated invariant T cells in hepatitis B virus-related liver failure

Xue

et al. 2020

WJG

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BACKGROUND Liver failure has high mortality and poor prognosis, and establishing new reliable markers for predicting its prognosis is necessary. Mucosal-associated invariant T (MAIT) cells are a novel population of innate-like lymphocytes involved in inflammatory liver disease, and their potential role in liver failure remains unclear. AIM To investigate alteration of circulating MAIT cells and assess its prognostic value in patients with hepatitis B virus (HBV)-related liver failure. METHODS We recruited 55 patients with HBV-related liver failure, 48 patients with chronic hepatitis B and 40 healthy controls (HCs) from Nantong Third People’s Hospital Affiliated to Nantong University. Peripheral blood mononuclear cells were isolated, and the percentage and number of circulating MAIT cells were detected by flow cytometry. Plasma levels of interleukin (IL)-7, IL-12p70, IL-18 and interferon-α were measured by Luminex assay. RESULTS Circulating MAIT cells were significantly decreased in HBV-related liver failure patients (percentage: 2.00 ± 1.22 vs 5.19 ± 1.27%, P < 0.0001; number: 5.47 ± 4.93 vs 84.43 ± 19.59, P < 0.0001) compared with HCs. More importantly, there was a significant reduction of MAIT cells in patients with middle/late-stage compared with early-stage liver failure. Circulating MAIT cells partially recovered after disease improvement, both in percentage (4.01 ± 1.21 vs 2.04 ± 0.95%, P < 0.0001) and in cell count (17.24 ± 8.56 vs 7.41 ± 4.99, P < 0.0001). The proportion (2.29 ± 1.01 vs 1.58 ± 1.38%, P < 0.05) and number (7.30 ± 5.70 vs 2.94 ± 1.47, P < 0.001) of circulating MAIT cells were significantly higher in the survival group than in the dead/liver transplantation group, and the Kaplan–Meier curve showed that lower expression of circulating MAIT cells (both percentage and cell count) predicted poor overall survival ( P < 0.01). Also, the levels of IL-12 (20.26 ± 5.42 pg/mL vs 17.76 ± 2.79 pg/mL, P = 0.01) and IL-18 (1470.05 ± 1525.38 pg/mL vs 362.99 ± 109.64 pg/mL, P < 0.0001) were dramatically increased in HBV-related liver failure patients compared with HCs. CONCLUSION Circulating MAIT cells may play an important role in the process of HBV-related liver failure and can be an important prognostic marker.

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Section: Discussionmentioning

confidence: 99%

Mucosal-associated invariant T cells in hepatitis B virus-related liver failure

Xue

et al. 2020

WJG

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“…A higher prevalence of NKT cells has been shown in the liver of PBC patients compared to healthy controls, as well as NK cells, that also contribute to cholangiocyte damage, autoantigen release and activation of autoreactive T lymphocytes [ 48 , 49 ]. Mucosal associated invariant T cells (MAIT cells), invariant mucosal T cells, are a relatively novel population of innate immune cells that produce inflammatory cytokines IFN-γ, TNF-α and IL-17, or independently, or by stimulation with microorganisms, present in a smaller percentage in the liver and blood of patients with PBC compared to controls [ 1 , 49 , 50 ].…”

Section: Immune Dysregulation In Pbcmentioning

confidence: 99%

Galectin-3 in Inflammasome Activation and Primary Biliary Cholangitis Development

Arsenijević

Stojanović

Milovanović

et al. 2020

IJMS

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Primary biliary cholangitis (PBC) is a chronic inflammatory autoimmune liver disease characterized by inflammation and damage of small bile ducts. The NLRP3 inflammasome is a multimeric complex of proteins that after activation with various stimuli initiates an inflammatory process. Increasing data obtained from animal studies implicate the role of NLRP3 inflammasome in the pathogenesis of various diseases. Galectin-3 is a β-galactoside-binding lectin that plays important roles in various biological processes including cell proliferation, differentiation, transformation and apoptosis, pre-mRNA splicing, inflammation, fibrosis and host defense. The multilineage immune response at various stages of PBC development includes the involvement of Gal-3 in the pathogenesis of this disease. The role of Galectin-3 in the specific binding to NLRP3, and inflammasome activation in models of primary biliary cholangitis has been recently described. This review provides a brief pathogenesis of PBC and discusses the current knowledge about the role of Gal-3 in NLRP3 activation and PBC development.

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“…Immunologists are currently debating whether all MAIT cells carry an invariant TCR α-chain. This invariant TCR α-chain is usually comprised of a T-cell receptor-α variable (TRAV) 1-2 region and a joining region in their T-cell receptor-α (TRAJ) that can be, in order of frequency: TRAJ33, TRAJ12, and TRAJ20 [ 30 , 31 , 32 , 33 , 34 ] ( Figure 1 ). Interestingly, the sequences of all of these TRAJ segments contain a tyrosine at position 95, which is involved in metabolite-antigen recognition by TRAJ33 [ 31 , 35 ].…”

Section: Classical Mait Cells With Trav1-2mentioning

confidence: 99%

MR1-Restricted T Cells in Cancer Immunotherapy

Flores-Villanueva

Sobhani

Wang

et al. 2020

Cancers

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Major histocompatibility complex class I-related (MR1) was first identified as a cell membrane protein involved in the development and expansion of a unique set of T cells expressing an invariant T-cell receptor (TCR) α-chain. These cells were initially discovered in mucosal tissues, such as the intestinal mucosa, so they are called mucosal-associated invariant T (MAIT) cells. MR1 senses the presence of intermediate metabolites of riboflavin and folic acid synthesis that have been chemically modified by the side-products of glycolysis, glyoxal or methylglyoxal. These modified metabolites form complexes with MR1 and translocate from the endoplasmic reticulum to the plasma membrane where MAIT cells’ TCRs recognize them. Recent publications report that atypical MR1-restricted cytotoxic T cells, differing from MAIT cells in TCR usage, antigen, and transcription factor profile, recognize an as yet unknown cancer-specific metabolite presented by MR1 in cancer cells. This metabolite may represent another class of neoantigens, beyond the neo-peptides arising from altered tumor proteins. In an MR1-dependent manner, these MR1-restricted T cells, while sparing noncancerous cells, kill many cancer cell lines and attenuate cell-line-derived and patient-derived xenograft tumors. As MR1 is monomorphic and expressed in a wide range of cancer tissues, these findings raise the possibility of universal pan-cancer immunotherapies that are dependent on cancer metabolites.

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Mucosal-Associated Invariant T cell in liver diseases

Cited by 18 publications

References 92 publications

Mucosal-associated invariant T cells in hepatitis B virus-related liver failure

Mucosal-associated invariant T cells in hepatitis B virus-related liver failure

Galectin-3 in Inflammasome Activation and Primary Biliary Cholangitis Development

MR1-Restricted T Cells in Cancer Immunotherapy

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