The Toll-like receptor 2 R753Q polymorphism defines a subgroup of patients with atopic dermatitis having severe phenotype

Ahmad-Nejad, Parviz; Mrabet-Dahbi, S.; Breuer, Kristine; Klotz, Martina; Werfel, Thomas; Herz, Udo; Heeg, Klaus; Neumaier, Michael; Renz, Harald

doi:10.1016/j.jaci.2003.12.583

Cited by 215 publications

(148 citation statements)

References 10 publications

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“…Genetic variations may exist in other skin barrier molecules or in the cutaneous immune response of AD. Molecular or cellular components for microbial sensing such as TLR (78)(79)(80), or skin tissue repair such as TSLP and ILC (28), deserve further studies. Prospective clinical studies are needed to correlate laboratory markers with development of moderate to severe AD and complications of AD.…”

Section: Discussionmentioning

confidence: 99%

New insights in the pathogenesis of atopic dermatitis

Ong

2013

Pediatr Res

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Section: Discussionmentioning

confidence: 99%

New insights in the pathogenesis of atopic dermatitis

Ong

2013

Pediatr Res

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“…13 The TLR2 Arg753Gln variant was chosen because it was shown to affect the response to bacterial peptides in vitro, 19 and to be associated with several immune pathologies. 11,21 The TLR4 Asp299Gly variant has been related to hyporesponsiveness to inhaled endotoxins in humans 12,20 and with several infectious and inflammatory conditions. 14,17,9 The TLR5 Arg392Stop variant in the ligand-binding domain abolished flagellin-induced signalling in CHO-K1 cells 57 and was associated with the susceptibility to Legionnaire's disease 15 and systemic Lupus erythematosus.…”

Section: Selection Of Polymorphismsmentioning

confidence: 99%

“…Some TLR gene variants with potential functional relevance have been associated with various phenotypes including susceptibility to infectious and inflammatory diseases as well as cancer. [11][12][13][14][15][16][17][18][19][20][21][22][23] First evidence links a polymorphism in TLR4 (Arg299Gly) with the susceptibility to gastric mucosaassociated lymphoid tissue (MALT) lymphoma. 16 Signalling through TLRs is involved not only in the primary induction of inflammation, however, also antiinflammatory mediators necessary for the resolution of inflammatory processes are activated.…”

Section: Introductionmentioning

confidence: 99%

Gene polymorphisms in Toll-like receptors, interleukin-10, and interleukin-10 receptor alpha and lymphoma risk

et al. 2006

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Interactions between environment and immune system play an essential role in the aetiology of immunopathologies, including lymphomas. Toll-like receptors (TLR) belong to a group of pattern recognition receptors, with importance for innate immune response and inflammatory processes. Interleukin-10 (IL-10) is a key regulatory cytokine and has been implicated in lymphomagenesis. Functional polymorphisms in these inflammation-associated genes may affect the susceptibility towards lymphoma. To test this hypothesis, we have genotyped DNA of 710 lymphoma cases and 710 controls within the context of a population-based epidemiological study for 11 functionally important single-nucleotide polymorphisms in TLR1, À2, À4, À5, À9, IL10 and IL10 receptor (IL10RA). The IL10RA Ser138Gly variant was underrepresented among lymphoma cases (odds ratio (OR) ¼ 0.81, 95 per cent confidence interval (95% CI) ¼ 0.65-1.02), mainly owing to an inverse association with Hodgkin's lymphoma (HL). The TLR2 À16933T4A variant was associated with a 2.8-fold increased risk of follicular lymphoma (95% CI ¼ 1.43-5.59) and a decreased risk of chronic lymphocytic leukaemia (OR ¼ 0.61, 95% CI ¼ 0.38-0.95). Furthermore, the TLR4 Asp299Gly variant was positively associated with the risk of mucosa-associated lymphoid tissue lymphoma (OR ¼ 2.76, 95% CI ¼ 1.12-6.81) and HL (OR ¼ 1.80, 95% CI ¼ 0.99-3.26). In conclusion, this study suggests an effect of polymorphisms in factors of the innate immune response in the aetiology of some lymphoma subtypes.

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“…TLR2 also can recognize lipopolysaccharide on some gram-negative bacteria, as well as fungi and possibly even herpes viruses [28,29]. In a study of 78 patients with mild to severe AD and 39 agematched healthy controls, it was found that genetic polymorphisms of TLR2 occurred in 11.5 % of AD patients and only 2.5 % of controls, and TLR2 polymorphism was associated with more severe AD [30]. Thus, some patients with AD have impaired aberrancies of innate immunity that may predispose them to increased microbial colonization and infection, aside from skin barrier defects.…”

Section: Cutaneous Infectionmentioning

confidence: 99%

Atopic Dermatitis: Update on Pathogenesis and Comorbidities

Silverberg

2012

Curr Derm Rep

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Atopic dermatitis (AD) is a significant cause of morbidity and healthcare costs in the United States and worldwide. The prevalence of AD in childhood is rising in the United States and other developed countries for reasons that are not well understood. Similarly, the prevalences of obesity and diabetes are on the rise, which might be contributing toward increased AD. This article reviews the association between AD and other atopic disorders with obesity and diabetes. Furthermore, recently recognized AD comorbidities, including fatty liver disease and erectile dysfunction, are reviewed. Potential mechanisms for the association between AD and metabolic disorders are discussed.

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The Toll-like receptor 2 R753Q polymorphism defines a subgroup of patients with atopic dermatitis having severe phenotype

Cited by 215 publications

References 10 publications

New insights in the pathogenesis of atopic dermatitis

New insights in the pathogenesis of atopic dermatitis

Gene polymorphisms in Toll-like receptors, interleukin-10, and interleukin-10 receptor alpha and lymphoma risk

Atopic Dermatitis: Update on Pathogenesis and Comorbidities

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