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Background: Psoriasis is a chronic, life-long inflammatory disorder that primarily affects the skin. The etiopathogenesis of psoriasis remains elusive. The activation of the NF-ҡB/Rel transcription family, by nuclear translocation of cytoplasmic complexes, plays a critical role in inflammation through its ability to induce transcription of pro-inflammatory genes. This pathway is activated upon appropriate cellular stimulation, most often by signals related to pathogens or stress.
Objective: To study TRAF3IP2 (rs33980500), TNFAIP3 (rs610604) and NFKBIA (rs12586317) gene activation single nucleotide polymorphisms are associated with risk of psoriasis in Chinese Han population of Wuhan city, Hubei Province.
Materials and Methods: The genetic analysis included samples from 44 patients and 50 controls was analyzed by Amplified Fragment Length Polymorphisms (AFLP System) using Applied Biosystems Gene Mapper 4.0.
Results: The average age of clients was 47 years with an age range of 9–86 years and an average age of onset of 37 years. 38 were male (86.36%) and 6 (13.64%) were female, of which six patients (13.64%) had a family history of psoriasis. The psoriasis area severity index (PASI) was about 10.7 (range 3.5-24), this scale evaluates the severity of three clinical signs (erythema, induration and desquamation) on a scale from 0 to 4 (from none to maximum). However, our research on the Chinese community yielded lack of association for the SNP rs12586317, rs33980500, and rs610604 with P-values of 0.9177, 0.3482, and 0.2009, respectively.
Conclusion: Genetic polymorphisms of NFKB1A (rs12586317), TRAF3IP2 (rs33980500) and TNFAIP3 (rs610604) were not associated with the susceptibility of psoriasis vulgaris in Chinese Han patients of Wuhan, Hubei province. However, the authors recommend a larger scale study.NF-kB is a key regulatory element in a variety of immune and inflammatory pathways, in cellular proliferation and differentiation and in apoptosis, thus, orchestrates inflammation and other complex biological processes in cells. Drugs that act on NF-kB will be key in the treatment of most chronic dermatoses.
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