The polymorphisms of Th1 cell surface gene Tim-3 are associated in a Korean population with rheumatoid arthritis

Chae, Soo-Cheon; Park, Young-Ran; Shim, Seung Cheol; Yoon, Kyung‐Sik; Chung, Hun‐Taeg

doi:10.1016/j.imlet.2004.06.008

Cited by 69 publications

(62 citation statements)

References 30 publications

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“…Previous studies using such approaches have demonstrated that the TIM-1 gene may be associated with susceptibility to allergic diseases and autoimmune diseases including RA in Korean (Chae et al, 2003(Chae et al, , 2004a(Chae et al, ,b, 2005, Chinese Han population (Liu et al, 2007;Wu et al, 2009a,b;Mou et al, 2010) and Japanese populations (Noguchi et al, 2003). In the present study, we analyzed four SNPs in the human TIM-1 gene of the Chinese Hui population.…”

Section: Discussionmentioning

confidence: 88%

“…Previous studies performed by Chae et al (2004aChae et al ( , 2005 have revealed direct correlations between specific TIM-1 allelic variants in the promoter region and exon 4 leading to increased susceptibility to RA in a Korean population. While recent studies demonstrated that the RA susceptibility of genetic variants of 4q27, 6q23, CCL21, TRAF1/C5, CD40, and PTPN22 in Caucasian populations they did not contribute significantly to RA in Koreans; this implies various genetic risk factors for RA to exist among different populations (Lee et al, 2009).…”

Section: Introductionmentioning

confidence: 91%

“…T-cell immunoglobulin domain and mucin domain (TIM) proteins have been reported to be expressed on T cells and are involved in the regulation of T helper (Th) cells immune responses and allergic diseases such as asthma and rheumatoid arthritis (RA) (Chae et al, 2003(Chae et al, , 2004a(Chae et al, , 2005Gao et al, 2005;Mou et al, 2010). The TIM gene family consists of eight genes on mouse chromosome 11B1.1, and three genes lie on the human chromosome 5q33.2.…”

Section: Introductionmentioning

confidence: 99%

“…Selective expression on Th2 cells may suggest that TIM-1 is a candidate susceptibility gene associated with Th cell-mediated allergic and autoimmune diseases. Recent population studies have demonstrated that genetic variations in TIM-1 were associated with susceptibility to both allergic diseases and autoimmune diseases (Chae et al, 2003(Chae et al, , 2004a(Chae et al, ,b, 2005Gao et al, 2005;Wu et al, 2009a,b). Furthermore, previous polymorphism studies performed on the TIM-1 promoter region in a Korean population have identified a promoter polymorphism, -1637A>G, to be associated with susceptibility to RA in a Korean population (Chae et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Polymorphisms of the TIM-1 gene are associated with rheumatoid arthritis in the Chinese Hui minority ethnic population

Xu¹,

Yang²,

Liu³

et al. 2012

Genet. Mol. Res.

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Section: Discussionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Polymorphisms of the TIM-1 gene are associated with rheumatoid arthritis in the Chinese Hui minority ethnic population

Xu¹,

Yang²,

Liu³

et al. 2012

Genet. Mol. Res.

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“…We have identified several SNPs which were associated with susceptibility to RA or SLE in Tim-3, Tim-1, Eotaxin-3, and FOXJ1 genes through the case-control association study in Korean population (Chae et al, 2004(Chae et al, , 2005aLi et al, 2007). In this study, we attempted a proteomic approach such as 2-DE and MALDI-TOF MS to find the candidate molecules for RA pathogenesis.…”

Section: Discussionmentioning

confidence: 99%

Polymorphisms of COTL1 gene identified by proteomic approach and their association with autoimmune disorders

et al. 2009

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To select candidate genes, we attempted to comparative analysis of protein levels between rheumatoid arthritis (RA) patients and healthy controls by two-dimensional electrophoresis (2-DE) and matrix-assisted laser desorption ionization mass spectrometry (MALDI-TOF-MS). We identified 17 proteins that showed up-or down-regulated spots in RA patients. We found that coactosin-like1 (COTL1) were highly expressed in RA patients compared with healthy controls. We performed a case-control study to determine whether the COTL1 gene polymorphisms were associated with RA and systemic lupus erythematosus (SLE). The genotype frequency of c.-1124G＞T and the allelic frequency of c.484G＞A in RA patients, and the genotype frequency of c.484G＞A in SLE patients were significantly different from healthy controls (P = 0.009, 0.027, and 0.025, respectively). We also investigated the correlation with the levels of rheumatoid factor (RF) and anti-cyclic citrullinated peptide (CCP) antibody in RA patients, and anti-nuclear antibodies (ANA) in SLE patients. The c.484G＞A polymorphism in RA patients has significant association with the levels of anti-CCP antibody (P = 0.03). Our findings demonstrated that c.-1124G＞T and c. 484G＞A polymorphisms of the COTL1 gene might be associated with the genetic susceptibility of autoimmune disorders.

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The role of immune regulatory molecules in rheumatoid arthritis: Implication for etiopathogenesis and prospective for treatment

Hemmatzadeh

Parvin

Mohammadi

et al. 2022

Journal Cellular Physiology

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Rheumatoid arthritis (RA) is considered an autoimmune chronic disorder and the most common inflammatory arthropathy. Disease progression in RA begins with asymptomatic autoimmune responses in cases with a genetic or environmental predisposition, that alters to arthralgia phase as autoantibodies reach the joints and subjects begin demonstrating nonspecific musculoskeletal presentations lacking any clinical symptoms of synovial inflammation. After that, patients' symptoms develop to undifferentiated arthritis (UA)/idiopathic arthritis (IA) whenever the subjects progress to clinical synovitis systemic comorbidities affecting the vasculature, metabolism, and bone, and eventually with augmented immune cell infiltration, IA/UA patients progress to clinically classifiable RA. RA is mainly correlated with different immune cells and each of them contributes variously to the pathogenesis of the disease. The pathogenesis of RA is altered by the contribution of both T and B cells in an autoimmune irregularity. Modulation of the immune responses occurs through regulatory and inhibitory molecules that control activation of the adaptive system as well as immune hemostasis. To confine the exorbitant T cell‐associated inflammatory reactions, the immune system provides a system of inhibitory feedbacks, collectively named immune checkpoints. In this review, we aimed to discuss about inhibitory members of immune checkpoint molecules, including programmed cell death 1 (PD‐1)/PD‐L1, cytotoxic‐T‐lymphocyte‐antigen‐4, lymphocyte activation gene‐3, T cell immunoglobulin‐3, V‐domain Ig suppressor of T cell activation, B‐ and T‐lymphocyte attenuator, and T cell immunoglobulin and ITIM domain and their role in RA.

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The polymorphisms of Th1 cell surface gene Tim-3 are associated in a Korean population with rheumatoid arthritis

Cited by 69 publications

References 30 publications

Polymorphisms of the TIM-1 gene are associated with rheumatoid arthritis in the Chinese Hui minority ethnic population

Polymorphisms of the TIM-1 gene are associated with rheumatoid arthritis in the Chinese Hui minority ethnic population

Polymorphisms of COTL1 gene identified by proteomic approach and their association with autoimmune disorders

The role of immune regulatory molecules in rheumatoid arthritis: Implication for etiopathogenesis and prospective for treatment

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