Nuclear Factor- kappa B (NF-ҡB) Activation Gene Single Nucleotide Polymorphisms (SNP) Associated with the Risk of Psoriasis in Chinese Han People of Wuhan, Hubei Province

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Malumani Malan
Wu Xuejingzi
Song Ji Quan


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.

Psoriasis, NF-kB, SNP, NFKB1A (rs12586317), TRAF3IP2 (rs33980500), TNFAIP3 (rs610604), Wuhan, Chinese population.

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Malan, M., Xuejingzi, W., & Quan, S. J. (2020). Nuclear Factor- kappa B (NF-ҡB) Activation Gene Single Nucleotide Polymorphisms (SNP) Associated with the Risk of Psoriasis in Chinese Han People of Wuhan, Hubei Province. Asian Journal of Research in Dermatological Science, 3(3), 46-55. Retrieved from
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Wu D, Wu Y, Liu JL, Wang B, Zhang XD. Association between HLA-Cw*0602 polymorphism and psoriasis risk: A meta-analysis. Genet Mol Res. 2011;10(4): 3109–3120.

Bronckers IMGJ, Paller AS, van Geel MJ, van de Kerkhof PCM, Seyger MMB. Psoriasis in children and adolescents: Diagnosis, management and comorbidities. Paediatr Drugs. 2015;17: 373–384.

Griffiths CE, Barker JN. Pathogenesis and clinical features of psoriasis. Lancet. 2007;370(9583):263–271.

Dogra S, Mahajan R. Psoriasis: Epidemiology, clinical features, co-morbidities and clinical scoring. Indian Dermatol Online J. 2016;7(6):471–480.

Nestle FO, Kaplan DH, Barker J. Psoriasis. N Engl J Med. 2009;361(5):496–509.

Yu P, Hao S, Zheng H, Zhao X, Li Y. Association of NLRP1 and NLRP3 polymorphisms with psoriasis vulgaris risk in the Chinese Han Population. Biomed Res Int.; 2018.

DOI: 10.1155/2018/4714836

Ding X, Wang T, Shen Y, Wang X, Zhou C, Tian S, et al. Prevalence of psoriasis in China: A population-based study in six cities. European Journal of Dermatology. 2012;22(5):663–667.

Gelfand JM, Feldman SR, Stern RS, Thomas J, Rolstad T, Margolis DJ. Determinants of quality of life in patients with psoriasis: A study from the US population. J Am Acad Dermatol. 2004;51(5):704–708.

Horn EJ, Fox KM, Patel V, Chiou C-F, Dann F, Lebwohl M. Association of patient-reported psoriasis severity with income and employment. J Am Acad Dermatol. 2007;57(6):963–971.

Di Meglio P, Villanova F, Nestle FO. Psoriasis. Cold Spring Harb Perspect Med. 2014;4(8).

DOI: 10.1101/cshperspect.a015354

Rahman P, Inman RD, Gladman DD, Reeve JP, Peddle L, Maksymowych WP. Association of interleukin-23 receptor variants with ankylosing spondylitis. Arthritis Rheum. 2008;58(4):1020–1025.

Clop A, Bertoni A, Spain SL, Simpson MA, Pullabhatla V, Tonda R, et al. An in-depth characterization of the major psoriasis susceptibility locus identifies candidate susceptibility alleles within an HLA-C enhancer element. PLoS One. 2013;8(8):e71690.

Hüffmeier U, Lascorz J, Becker T, Schürmeier-Horst F, Magener A, Ekici AB, et al. Characterisation of psoriasis susceptibility locus 6 (PSORS6) in patients with early onset psoriasis and evidence for interaction with PSORS1. J Med Genet. 2009;46(11):736–744.

González S, Martínez-Borra J, López-Vázquez A, García-Fernández S, Torre-Alonso JC, López-Larrea C. MICA rather than MICB, TNFA, or HLA-DRB1 is associated with susceptibility to psoriatic arthritis. The Journal of Rheumatology. 2002;29(5):973–978.

Cargill M, Schrodi SJ, Chang M, Garcia VE, Brandon R, Callis KP, et al. A large-scale genetic association study confirms IL12B and leads to the identification of IL23R as psoriasis-risk genes. Am J Hum Genet. 2007;80(2):273–290.

Capon F, Di Meglio P, Szaub J, Prescott NJ, Dunster C, Baumber L, et al. Sequence variants in the genes for the interleukin-23 receptor (IL23R) and its ligand (IL12B) confer protection against psoriasis. Hum Genet. 2007;122(2):201–206.

Wolf N, Quaranta M, Prescott NJ, Allen M, Smith R, Burden AD, et al. Psoriasis is associated with pleiotropic susceptibility loci identified in type II diabetes and Crohn disease. J Med Genet. 2008;45(2):114–116.

Li Y, Liao W, Chang M, Schrodi SJ, Bui N, Catanese JJ, et al. Further genetic evidence for three psoriasis-risk genes: ADAM33, CDKAL1, and PTPN22. J Invest Dermatol. 2009;129(3):629–634.

Sugiura K, Muto M, Akiyama M. CARD14 c.526G>C (p.Asp176His) is a significant risk factor for generalized pustular psoriasis with psoriasis vulgaris in the Japanese cohort. J Invest Dermatol. 2014;134(6):1755–1757.

Howes A, O’Sullivan PA, Breyer F, Ghose A, Cao L, Krappmann D, et al. Psoriasis mutations disrupt CARD14 autoinhibition promoting BCL10-MALT1-dependent NF-κB activation. Biochem J. 2016;473(12): 1759–1768.

Inzinger M, Wippel-Slupetzky K, Weger W, Richter L, Mlynek A, Fleischander B, et al. Survival and effectiveness of tumour necrosis factor-alpha inhibitors in the treatment of plaque psoriasis under daily life conditions: Report from the psoriasis registry Austria. Acta Derm Venereol. 2016;96(2):207–212.

Talamonti M, Botti E, Galluzzo M, Teoli M, Spallone G, Bavetta M, et al. Pharmacogenetics of psoriasis: HLA-Cw6 but not LCE3B/3C deletion nor TNFAIP3 polymorphism predisposes to clinical response to interleukin 12/23 blocker ustekinumab. Br J Dermatol. 2013;169(2): 458–463.

Villarreal-MartíNez A, Gallardo-Blanco H, Cerda-Flores R, Torres-MuñOz I, GóMez-Flores M, Salas-AlaníS J, et al. Candidate gene polymorphisms and risk of psoriasis: A pilot study. Experimental and Therapeutic Medicine. 2016;11(4):1217–1222.

Feng B-J, Sun L-D, Soltani-Arabshahi R, Bowcock AM, Nair RP, Stuart P, et al. Multiple Loci within the major histocompatibility complex confer risk of psoriasis. PLoS Genet. 2009;5(8): e1000606.

Koutruba N, Emer J, Lebwohl M. Review of ustekinumab, an interleukin-12 and interleukin-23 inhibitor used for the treatment of plaque psoriasis. Ther Clin Risk Manag. 2010;6:123–141.

Baldwin AS. The NF-kappa B and I kappa B proteins: New discoveries and insights. Annu Rev Immunol. 1996;14:649–683.

Chiricozzi A, Romanelli P, Volpe E, Borsellino G, Romanelli M. Scanning the immuno pathogenesis of psoriasis. Int J Mol Sci. 2018;19(1).

DOI: 10.3390/ijms19010179

Jankowiak B, Krajewska-Kulak E, Van Damme-Ostapowicz K, Wronska I, Lukaszuk C, Niczyporuk W, et al. The need for health education among patients with psoriasis. Dermatol Nurs. 2004;16(5): 439–444.

Rahman P, Elder JT. Genetics of psoriasis and psoriatic arthritis: A REPORT FROM THE GRAPPA 2010 annual meeting. J Rheumatol. 2012;39(2):431–433.

Prieto-Pérez R, Solano-López G, Cabaleiro T, Román M, Ochoa D, Talegón M, et al. Polymorphisms associated with age at onset in patients with moderate-to-severe plaque psoriasis. J Immunol Res. 2015;101879.

Arifin W, Zahiruddin W. Sample size calculation in animal studies using resource equation approach. - PubMed - NCBI.


(Accessed 6 June 2018)

Kadam P, Bhalerao S. Sample size calculation. Int J Ayurveda Res. 2010;1(1):55–57.

Pourhoseingholi MA, Vahedi M, Rahimzadeh M. Sample size calculation in medical studies. Gastroenterol Hepatol Bed Bench. 2013;6(1):14–17.

Lawrence T. The nuclear factor NF-κB pathway in inflammation. Cold Spring Harb Perspect Biol. 2009;1(6).

DOI: 10.1101/cshperspect.a001651

Qureshi AA, Dominguez PL, Choi HK, Han J, Curhan G. Alcohol intake and risk of incident psoriasis in US women: A prospective study. Arch Dermatol. 2010;146(12):1364–1369.

Poikolainen K, Reunala T, Karvonen J, Lauharanta J, Kärkkäinen P. Alcohol intake: A risk factor for psoriasis in young and middle aged men? BMJ. 1990;300(6727):780–783.

Behnam SM, Behnam SE, Koo JY. Alcohol as a risk factor for plaque-type psoriasis. Cutis. 2005;76(3):181–185.

Xhaja A, Shkodrani E, Frangaj S, Kuneshka L, Vasili E. An epidemiological study on trigger factors and quality of life in psoriatic patients. Mater Sociomed. 2014;26(3):168–171.

Tieri P, Termanini A, Bellavista E, Salvioli S, Capri M. Charting the NF-kB pathway interactome map. PLoS ONE. 2012;7(3):11.

Tak PP, Firestein GS. NF-κB: A key role in inflammatory diseases. J Clin Invest. 2001;107(1):7–11.

Karin M, Ben-Neriah Y. Phosphorylation meets ubiquitination: The control of NF-[kappa]B activity. Annu Rev Immunol. 2000;18:621–663.

Senftleben U, Cao Y, Xiao G, Greten FR, Krähn G, Bonizzi G, et al. Activation by IKKalpha of a second, evolutionary conserved, NF-kappa B signaling pathway. Science. 2001;293(5534):1495–1499.

Dejardin E, Droin NM, Delhase M, Haas E, Cao Y, Makris C, et al. The lymphotoxin-beta receptor induces different patterns of gene expression via two NF-kappaB pathways. Immunity. 2002;17(4):525–535.

Bonizzi G, Bebien M, Otero DC, Johnson-Vroom KE, Cao Y, Vu D, et al. Activation of IKKalpha target genes depends on recognition of specific kappaB binding sites by RelB: p52 dimers. EMBO J. 2004;23(21):4202–4210.

Novack DV, Yin L, Hagen-Stapleton A, Schreiber RD, Goeddel DV, Ross FP, et al. The IkappaB function of NF-kappaB2 p100 controls stimulated osteoclastogenesis. J Exp Med. 2003;198(5):771–781.

Ellinghaus E, Ellinghaus D, Stuart PE, Nair RP, Debrus S, Raelson JV, et al. Genome-wide association study identifies a psoriasis susceptibility locus at TRAF3IP2. Nat Genet. 2010;42(11):991–995.

Lowes MA, Kikuchi T, Fuentes-Duculan J, Cardinale I, Zaba LC, Haider AS, et al. Psoriasis vulgaris lesions contain discrete populations of Th1 and Th17 T cells. J Invest Dermatol. 2008;128(5):1207–1211.

Hunter CA. Act1-ivating IL-17 inflammation. Nat Immunol. 2007;8(3): 232–234.

Stuart PE, Nair RP, Ellinghaus E, Ding J, Tejasvi T, Gudjonsson JE, et al. Genome-wide association analysis identifies three psoriasis susceptibility loci. Nat Genet. 2010;42(11):1000–1004.

Indhumathi S, Thappa DM, Negi VS, Rajappa M, Chandrashekar L, Ananthanarayanan PH. TNFAIP3 and TNIP1 polymorphisms confer psoriasis risk in South Indian Tamils. - PubMed - NCBI. TNFAIP3 and TNIP1 polymorphisms confer psoriasis risk in South Indian Tamils.


(Accessed 6 July 2019)

Goldminz AM, Au SC, Kim N, Gottlieb AB, Lizzul PF. NF-κB: An essential transcription factor in psoriasis. J Dermatol Sci. 2013;69(2):89–94.