A functional candidate screen for coeliac disease genes

Curley, Christine R.; Monsuur, Alienke J.; Wapenaar, Martin C.; Rioux, John D.; Wijmenga, Cisca

doi:10.1038/sj.ejhg.5201687

Cited by 29 publications

(31 citation statements)

References 35 publications

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“…CYP4F enzymes are also expressed in neurons and glia, and LTB 4 hydroxylase activity limits neuroinflammation in mouse models (Sehgal et al, 2011). Genetic association studies link variants of the CYP4F3 and CYP4F2 genes with celiac disease and Crohn's disease, inflammatory disorders of the gastrointestinal tract (Costea et al, 2010;Curley, Monsuur, Wapenaar, Rioux, & Wijmenga, 2006). The relevance of LTB 4 inactivation is inferred from studies that showed reduced LTB 4 ω-hydroxylase activity in neutrophils and colonic mucosa from patients with IBD (Ikehata et al, 1995).…”

Section: Ltb 4 Inactivationmentioning

confidence: 99%

Role of Cytochrome P450s in Inflammation

Christmas

2015

Advances in Pharmacology

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Section: Ltb 4 Inactivationmentioning

confidence: 99%

Role of Cytochrome P450s in Inflammation

Christmas

2015

Advances in Pharmacology

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“…CYP4F3 and CYP4F2 catalyse the inactivation of leukotriene B4 (LTB4), a potent mediator of inflammation responsible for recruitment and activation of neutrophils. 97 Additionally on chromosome 19, a certain combination of expressed killer cell immunoglobulin-like receptor two (KIR2DL5) genotypes has shown association in a Spanish population of 413 cases and 231 controls. 98 The candidate gene approach searching for non-HLA genes in CD Cytotoxic T-lymphocyte-associated protein: CTLA4 (CELIAC 3) CTLA4 plays an important role in maintaining tolerance to self-antigens, both as a negative regulator of T-cell Searching for genes influencing coeliac disease Å T Naluai et al proliferation through the co-stimulatory signal and as an inducer of clonal anergy.…”

Section: Fine-mapping and Positional Candidates On Chromosomes 5 And 19mentioning

confidence: 99%

Searching for genes influencing a complex disease: the case of coeliac disease

et al. 2007

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Recently, a few genes have been reported to be causative in inflammatory diseases. Still, we are waiting for the vast majority to be discovered. New tools for genotyping and statistical analysis have been developed and emphasis has been put on study design. Coeliac disease (CD) is a disorder, where prolamins in dietary wheat gluten and related proteins from rye or barley are not tolerated. It is one of the most common chronic diseases in humans exceeding a population prevalence of 1%. In this article, we will summarise what is currently known about the genetics influencing CD with the emphasis on the non-HLA genetic component. We will discuss some difficulties when searching for susceptibility genes in disorders with complex inheritance patterns.

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“…However, susceptibility caused by MYO9B was not replicated in additional populations [2][3][4], including in our Spanish population [5], and its role as the disease-causinggene at CELIAC4 has been questioned [6]. Curley and colleagues [7] indicated two additional genes in this region with small effects in CD risk in the Dutch population, CYP4F3 and CYP4F2, but no replication confirmed this association either. An additional candidate gene on 19p13 is ICAM1, which encodes the immunoglobulin-like intercellular adhesion molecule ICAM-1 (CD54) that mediates interactions between cells through binding to its natural ligands, lymphocyte functionassociated antigen-1 (LFA-1) and Mac-1.…”

Section: Introductionmentioning

confidence: 81%