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Association analysis of GWAS and candidate gene loci in a Pakistani population with psoriasis.

Saeeda Munir ; Simeen Ber Rahman ; Sadia Rehman ; Nusrat Saba ; Wasim Ahmad ; Staffan Nilsson (Institutionen för matematiska vetenskaper, matematisk statistik) ; Kehkashan Mazhar ; Åsa Torinsson Naluai
Molecular immunology (1872-9142). Vol. 64 (2015), 1, p. 190-4.
[Artikel, refereegranskad vetenskaplig]

Psoriasis is a common inflammatory and hyper proliferative condition of the skin and a serious chronic systemic autoimmune disease. We undertook an association study to investigate the genetic etiology of psoriasis in a Pakistani population by genotyping single-nucleotide polymorphisms (SNPs) previously reported to be associated in genome-wide association (GWAS) or in candidate gene studies of psoriasis. Fifty seven single-nucleotide polymorphisms (SNPs) from 42 loci were genotyped in 533 psoriasis patients and 373 controls. Our results showed genome wide significant association of the MHC region (rs1265181 being the most significant from five SNPs used with overall OR=3.38; p=2.97E-18), as well as nominally significant associations at ten other loci (p<0.05) in the Pakistani population (LCE3B, REL, IL13/IL4, TNIP1, IL12B, TRAF3IP2, ZC3H12C, NOS2 and RNF114 from GWAS and PRR9 from a previous candidate gene study). Overall, only nine SNPs out of the 42 GWAS loci, displayed an odds ratio in the opposite allelic direction and only three did not reach similar odds ratio within 95% confidence interval as previously reported (SLC45A1/TNFRSF9, ELMO1 and IL28RA). This indicates similar genetic risk factors and molecular mechanisms behind disease in Pakistani psoriasis patients as in other populations. In addition, we show that the MHC and TNIP1 regions are significantly different in patients with psoriasis onset before the age of 40 (type I) compared to after 40 years of age (type II). MHC being associated mainly with type I while TNIP1 with type II patients.

Nyckelord: Autoimmunity; Psoriasis; Systemic immunity; Molecular mechanisms; Genetic risk factors; HLA



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Denna post skapades 2015-01-18. Senast ändrad 2015-02-19.
CPL Pubid: 210947

 

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Institutioner (Chalmers)

Institutionen för matematiska vetenskaper, matematisk statistik (2005-2016)
Institutionen för biomedicin, avdelningen för medicinsk genetik och klinisk genetik (GU)

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Molekylär medicin (genetik och patologi)

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