CTLA4 Gene Polymorphisms in Dutch and Chinese Patients with Inflammatory Bowel Disease

Xiu-juan, Bai; Jb, Crusius; Wu, Jianqing; Zwiers, Antonie; Aa, van Bodegraven; Peña, A. S.

doi:10.1080/003655202761020579

Cited by 46 publications

(48 citation statements)

References 31 publications

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“…Nevertheless, our study was underpowered to detect smaller effects such as an OR of 1.14 associated with type 1 diabetes [13]. Interestingly, our data are in accordance with those obtained in a study of IBD in a Dutch Caucasian population in which no association between ϩ49A/G and C-318T CTLA4 polymorphisms and IBD was observed [22]. These findings and our results suggest that CTLA4 polymorphism does not play a major role in IBD susceptibility.…”

Section: Discussionsupporting

confidence: 94%

CTLA4/CT60 polymorphism is not relevant in susceptibility to autoimmune inflammatory intestinal disorders

et al. 2005

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Section: Discussionsupporting

confidence: 94%

CTLA4/CT60 polymorphism is not relevant in susceptibility to autoimmune inflammatory intestinal disorders

et al. 2005

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“…Thus, IL-2-deficient T cells have reduced CTLA-4 expression but increased production of RANKL, and these two defects seem responsible for lymphoaccumulation and AHA, or osteopenia and IBD, respectively. Consistent with the lack of correlation between reduced CTLA-4 expression and IBD, CTLA-4-deficient mice do not develop IBD (M.-L. Alegre, unpublished observation; data not shown), and CTLA-4 polymorphisms have not been associated with IBD in humans (40).…”

Section: Discussionmentioning

confidence: 54%

Transgenic Expression of CTLA-4 Controls Lymphoproliferation in IL-2-Deficient Mice

Hwang

Sweatt

Mashayekhi

et al. 2004

The Journal of Immunology

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IL-2-deficient mice develop a lymphoproliferative and autoimmune disease characterized by autoimmune hemolytic anemia (AHA) and inflammatory bowel disease. We have previously reported that IL-2 is necessary for optimal up-regulation of CTLA-4, an inducible negative regulator of T cell activation. In this study, we have tested the hypothesis that reduced expression of CTLA-4 in IL-2-deficient T cells contributes to the pathogenesis of disease in IL-2-deficient mice. Expression of CTLA-4 as a transgene completely prevented lymphoaccumulation and AHA in IL-2-deficient mice. The normalization of T cell numbers was due to inhibition of expansion of conventional CD4+CD25− T cells rather than to rescue of the numbers or function of CD4+CD25+ regulatory T cells, suggesting that CTLA-4 expression on conventional T cells plays a role in maintaining normal T cell homeostasis. In addition, the inhibitory effect of the CTLA-4 transgene on T cell expansion was at least in part independent of CD28 expression. Our results suggest that deficient CTLA-4 expression on conventional T cells contributes to the pathophysiology of the lymphoproliferative disease and AHA in IL-2-deficient mice. Thus, restoring CTLA-4 expression in T cells may be an attractive strategy to control clinical autoimmune diseases in which CTLA-4 expression is reduced.

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“…In addition, a study from Oxford compared 645 CD patients with 1190 controls and showed an association of ATG16L1 with CD [14] . To understand fully the function of this gene, a study utilized oligo-based silencing RNA directed against ATG16L1 isoforms, where autophagy was induced by Salmonella typhimurium in ATG16L1 knockdown HEK293 cells.…”

Section: Autophagy-related 16-like 1 Protein Complexmentioning

confidence: 98%

Role ofATG16L,NOD2andIL23Rin Crohn’s disease pathogenesis

Naser

Arce²,

Khaja³

et al. 2012

WJG

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Inflammatory bowel disease is a group of diseases that includes Crohn's disease (CD) and ulcerative colitis. CD is characterized as a chronic inflammatory disease of the gastrointestinal tract, ranging from the mouth to the anus. Although there are gross pathological and histological similarities between CD and Johne's disease of cattle, the cause of CD remains controversial. It is vital to understand fully the cause of this disease because it affects approximately 500,000 people in North America and Europe. It ranges from 27 to 48 cases per 100,000 people. There are many theories on the cause of CD ranging from possible association with environmental factors including microorganisms to imbalance in the intestinal normal flora of the patients. Regardless of the environmental trigger, there is strong evidence that a genetic disposition is a major key in acquiring CD. Many studies have proven the link between mutations in the ATG16L, NOD2/CARD15, IBD5, CTLA4, TNFSF15 and IL23R genes, and CD. The purpose of this review is to examine all genetic aspects and theories of CD, including up to date multiple population studies performed worldwide.

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CTLA4 Gene Polymorphisms in Dutch and Chinese Patients with Inflammatory Bowel Disease

Abstract: C-318T and A+49G CTLA4 gene polymorphisms and their haplotypes are not associated in Dutch Caucasian patients with IBD and in Chinese patients with UC.

Cited by 46 publications

References 31 publications

CTLA4/CT60 polymorphism is not relevant in susceptibility to autoimmune inflammatory intestinal disorders

CTLA4/CT60 polymorphism is not relevant in susceptibility to autoimmune inflammatory intestinal disorders

Transgenic Expression of CTLA-4 Controls Lymphoproliferation in IL-2-Deficient Mice

Role ofATG16L,NOD2andIL23Rin Crohn’s disease pathogenesis

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