T-Cell Regulatory Gene CTLA-4 Polymorphism/Haplotype Association with Autoimmune Pancreatitis

Chang, Ming‐Chu; Chang, Yu-Ting; Tien, Yu‐Wen; Liang, Po-Chin; Jan, I-Shiow; Wei, Shu–Chen; Wong, Jau‐Min

doi:10.1373/clinchem.2007.085951

Cited by 135 publications

(86 citation statements)

References 41 publications

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“…Hereafter, the concept of AIP has been widely accepted, and its clinical, histologic, radiographic, and serologic features have been characterized [5][6][7][8][9][10][11][12] . The cellular mechanisms and genetic factors contributing to AIP are also investigated [17][18][19] .…”

Section: Discussionmentioning

confidence: 99%

Diagnosis and management of autoimmune pancreatitis: Experience from China

Song

Liu²,

Zhou³

et al. 2008

WJG

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Section: Discussionmentioning

confidence: 99%

Diagnosis and management of autoimmune pancreatitis: Experience from China

Song

Liu²,

Zhou³

et al. 2008

WJG

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“…A possible genetic association between CTLA-4 polymorphism and AIP has been shown [62,64]. In addition, a recent study has shown that serum sCTLA-4 levels are increased in AIP [62].…”

Section: Sctla-4 and Autoimmune Diseasesmentioning

confidence: 98%

The soluble CTLA-4 receptor and its role in autoimmune diseases: an update

Saverino

Simone

Bagnasco

et al. 2010

Autoimmun Highlights

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CTLA-4, initially described as a membranebound molecule, is a costimulatory receptor transducing a potent inhibitory signal. Increasing evidence shows the CTLA-4 gene to be an important susceptibility locus for autoimmune endocrinopathies and other autoimmune disorders. A soluble form of cytotoxic T-lymphocyte-associated antigen-4 (sCTLA-4) has been established and shown to possess CD80/CD86 binding activity and in vitro immunoregulatory functions. sCTLA-4 is generated by alternatively spliced mRNA. Whereas low levels of sCTLA-4 are detected in normal human serum, increased serum levels are observed in several autoimmune diseases (e.g. Graves’ disease, myasthenia gravis, systemic lupus erythematosus, type 1 diabetes, systemic sclerosis, coeliac disease, autoimmune pancreatitis and primary biliary cirrhosis). The biological significance of increased sCTLA-4 serum levels is not fully clarified yet. On the one hand, it can be envisaged that sCTLA-4 specifically inhibits early T-cell activation by blocking the interaction of CD80/CD86 with the costimulatory receptor CD28. On the other hand, higher levels of sCTLA-4 could compete for the binding of the membrane form of CTLA-4 with CD80/CD86 in the later phases of T-lymphocyte activation, causing a reduction in inhibitory signalling. This double-edged nature of sCTLA-4 to block the binding of CD28 to CD80/CD86 may result in different outcomes during the clinical course of an autoimmune disease.

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“…Five non-HLA genes, single-nucleotide polymorphisms (SNP) in which are associated with disease development and/or higher disease activity, are cytotoxic T lymphocyte-associated protein 4 (CTLA4), tumor necrosis factor (TNF), Fc receptor-like 3 (FCRL3), trypsin 1 (PRSS1), and cystic fibrosis transmembrane conductance regulator (CFTR) [97][98][99][100][101]. More comprehensive analyses such as genome-wide association studies (GSWAs) are needed in order to more fully understand the genetic risks of this condition.…”

Section: Genetic Risksmentioning

confidence: 99%

IgG4-related sclerosing cholangitis: all we need to know

2016

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Our knowledge and experience of IgG4-related sclerosing cholangitis (ISC) have expanded in the last decade. ISC is one of the common organ manifestations of IgG4-related disease (IgG4-RD); approximately 60 % of patients with this systemic condition have ISC in the proximal and/or distal bile ducts. ISC needs to be discriminated from primary sclerosing cholangitis, cholangiocarcinoma, and other rare forms of lymphoplasmacytic cholangiopathy (e.g., follicular cholangitis and sclerosing cholangitis with granulocytic epithelial lesions). Its diagnosis requires a multidisciplinary approach, in which serology, histology, and imaging play crucial roles. Treatments with high-dose corticosteroids typically lead to the rapid and consistent induction of disease remission. Another promising therapeutic approach is B-cell depletion with rituximab. Although disease relapse is relatively common, provided that appropriate treatments are administered, ISC is considered a ''benign'' disease with a low risk of liver failure and biliary malignancy. Its molecular pathology is characterized by Th2-dominant immune reactions, regulatory T-cell activation, and CCL1-CCR8 interactions. Particular subsets of B cells such as plasmablasts and regulatory B cells also expand. A recent global proteomic study demonstrated that three significantly activated immunological cascades in ISC were all B-cell-or immunoglobulin-related (Fc-gamma receptormediated phagocytosis, B-cell receptor signaling pathway, and Fc-epsilon receptor I signaling pathway), suggesting the crucial roles of B cells in the underlying immune reactions. Despite the expansion of our knowledge of the pathophysiology of ISC, the exact role of IgG4 remains unclear. A better understanding of its immunopathology will offer some potential drug targets for this emerging biliary disease.

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T-Cell Regulatory Gene CTLA-4 Polymorphism/Haplotype Association with Autoimmune Pancreatitis

Cited by 135 publications

References 41 publications

Diagnosis and management of autoimmune pancreatitis: Experience from China

Diagnosis and management of autoimmune pancreatitis: Experience from China

The soluble CTLA-4 receptor and its role in autoimmune diseases: an update

IgG4-related sclerosing cholangitis: all we need to know

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