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      TIM-3 rs1036199 polymorphism increases susceptibility to autoimmune diseases: evidence based on 4200 subjects

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          Abstract

          Conflicting results have been reported regarding differing studies on the association between T-cell immunoglobulin and mucin domain 3 polymorphisms and autoimmune disease. The purpose of the present study was to evaluate the association of TIM-3 rs1036199 (4259 G/T) polymorphism with autoimmune disease susceptibility. A meta-analysis was performed to obtain a more precise evaluation of the association. Ten eligible studies were retrieved by searching PubMed, Embase and Web of Science databases, and statistical analyses were performed using STATA software. The pooled results indicated that TIM-3 rs1036199 polymorphism was significantly associated with an increased risk of overall autoimmune disease in allele comparison (G versus T: OR = 1.59, 95%CI: 1.17–2.17) and heterozygous comparison (GT versus TT: OR = 1.68, 95%CI: 1.37–2.06). Subgroup analyses based on disease type demonstrated that TIM-3 rs1036199 polymorphism was associated with an increased risk of rheumatic arthritis (G versus T: OR = 1.88, 95%CI: 1.45–2.44; GT versus TT: OR = 2.02, 95%CI: 1.53–2.65), especially in Asian populations.

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          Interaction of Tim-3 and Tim-3 ligand regulates T helper type 1 responses and induction of peripheral tolerance.

          Catherine Sabatos, Sumone Chakravarti, Eugene Cha … (2003)
          T helper type 1 (T(H)1) immune responses are central in cell-mediated immunity, and a T(H)1-specific cell surface molecule called Tim-3 (T cell immunoglobulin domain, mucin domain) has been identified. Here we report the identification of a secreted form of Tim-3 that contains only the immunoglobulin (Ig) variable (V) domain of the full-length molecule. Fusion proteins (Tim-3-Ig) of both Tim-3 isoforms specifically bound CD4(+) T cells, indicating that a Tim-3 ligand is expressed on CD4(+) T cells. Administration of Tim-3-Ig to immunized mice caused hyperproliferation of T(H)1 cells and T(H)1 cytokine release. Tim-3-Ig also abrogated tolerance induction in T(H)1 cells, and Tim-3-deficient mice were refractory to the induction of high-dose tolerance. These data indicate that interaction of Tim-3 with Tim-3 ligand may serve to inhibit effector T(H)1 cells during a normal immune response and may be crucial for the induction of peripheral tolerance.
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            Detecting shared pathogenesis from the shared genetics of immune-related diseases.

            Cisca Wijmenga, Alexandra Zhernakova, Thomas Gent (2008)
            Recent genetic studies have revealed shared immunological mechanisms in several immune-related disorders that further our understanding of the development and concomitance of these diseases. Our Review focuses on these shared aspects, using the novel findings of recently performed genome-wide association studies and non-synonymous SNP scans as a starting point. We discuss how identifying new genes that are associated with more than one autoimmune or chronic inflammatory disorder could explain the genetic basis of the shared pathogenesis of immune-related diseases. This analysis helps to highlight the key molecular pathways that are involved in these disorders and the potential roles of novel genes in immune-related diseases.
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              PD-1 and Tim-3 regulate the expansion of tumor antigen-specific CD8⁺ T cells induced by melanoma vaccines.

              Julien Fourcade, Zhaojun Sun, Ornella Pagliano … (2014)
              Although melanoma vaccines stimulate tumor antigen-specific CD8(+) T cells, objective clinical responses are rarely observed. To investigate this discrepancy, we evaluated the character of vaccine-induced CD8(+) T cells with regard to the inhibitory T-cell coreceptors PD-1 and Tim-3 in patients with metastatic melanoma who were administered tumor vaccines. The vaccines included incomplete Freund's adjuvant, CpG oligodeoxynucleotide (CpG), and the HLA-A2-restricted analog peptide NY-ESO-1 157-165V, either by itself or in combination with the pan-DR epitope NY-ESO-1 119-143. Both vaccines stimulated rapid tumor antigen-specific CD8(+) T-cell responses detected ex vivo, however, tumor antigen-specific CD8(+) T cells produced more IFN-γ and exhibited higher lytic function upon immunization with MHC class I and class II epitopes. Notably, the vast majority of vaccine-induced CD8(+) T cells upregulated PD-1 and a minority also upregulated Tim-3. Levels of PD-1 and Tim-3 expression by vaccine-induced CD8(+) T cells at the time of vaccine administration correlated inversely with their expansion in vivo. Dual blockade of PD-1 and Tim-3 enhanced the expansion and cytokine production of vaccine-induced CD8(+) T cells in vitro. Collectively, our findings support the use of PD-1 and Tim-3 blockades with cancer vaccines to stimulate potent antitumor T-cell responses and increase the likelihood of clinical responses in patients with advanced melanoma. ©2013 AACR.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Biosci Rep
                Journal ID (iso-abbrev): Biosci. Rep
                Journal ID (hwp): ppbioscirep
                Journal ID (publisher-id): BSR
                Title: Bioscience Reports
                Publisher: Portland Press Ltd.
                ISSN (Print): 0144-8463
                ISSN (Electronic): 1573-4935
                Publication date (Electronic preprint): 30 October 2018
                Publication date Collection: 21 December 2018
                Publication date (Electronic): 23 November 2018
                Volume: 38
                Issue: 6
                Electronic Location Identifier: BSR20181235
                Affiliations
                [1 ]Department of Immunology, Medical College, Henan University of Science and Technology, Luoyang 471023, China
                [2 ]Network Information Center, Henan University of Science and Technology, Luoyang 471023, China
                Author notes
                Correspondence: Rongzeng Liu ( rongzengliu@ 123456outlook.com )
                Author information
                http://orcid.org/0000-0002-0518-6145
                Article
                DOI: 10.1042/BSR20181235
                PMC ID: 6250810
                PubMed ID: 30377229
                SO-VID: b07c24c7-58e5-4da2-bf28-f8692fe7d271
                Copyright © © 2018 The Author(s).
                License:

                This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).

                History
                Date received : 23 July 2018
                Date revision received : 23 October 2018
                Date accepted : 29 October 2018
                Page count
                Pages: 8
                Categories
                Subject: Research Articles
                Subject: Research Article
                Subject: 42
                Subject: 45
                Subject: 15

                ScienceOpen disciplines: Life sciences
                Keywords: autoimmune diseases,meta-analysis,polymorphism,tim-3
                Data availability:
                ScienceOpen disciplines: Life sciences
                Keywords: autoimmune diseases, meta-analysis, polymorphism, tim-3

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