HLA-DQA1 and HLA-DQB1 genotyping among lichen planus patients in Basrah‏ ‏province ‎


Background: Lichen planus is an inflammatory, pruritic disease of the skin and mucus membranes, which can be ‎either generalized or localized. Many studies indicated that human leukocyte antigens might have a role in lichen ‎planus (LP). As far as my knowledge, no previous study had done in Iraq about HLA-DQA1 and -DQB1 alleles ‎frequencies in patients with lichen planus. ‎Aim: The aim of the present study is to investigate the additional genetic contribution to lichen planus susceptibility ‎lying on the HLA region, by focusing on the possible differential contribution of the different DQA1 and DQB1 carrying ‎haplotypes.‎Method: The present study was carried out in College of Medicine during the period between (2012-2014). 50 patients ‎with lichen planus attending Basrah General Hospital and private clinic, and 50 healthy controls‏ ‏were included in the ‎study, with age group from (13-67) years. 100 DNA samples were purified from the blood samples of patients and ‎controls, and then followed by PCR amplification of HLA-DQA1 and DQB1 genes in Cell Research Unit, Biology ‎Department, College of Science, University of Basrah. The sequencing-PCR was done in Korea, Bioneer sequencing ‎laboratories. ‎Results & Conclusions: Results indicated statistically significant decreased frequencies of HLA-DQA1*010201 ‎‎(P<0.005), DQA1*0201 (P < 0.05), and -DQB1*030201 (P < 0.005) alleles in lichen planus patients, which indicated ‎that these alleles might be a protective factors. Results also indicated statistically significant increased frequencies of ‎DQA1*010401 (P<0.005), DQA1*040101 (P<0.005) DQA1*050101 (P<0.005), DQB1*030101 (P<0.005) and ‎DQB1*050101 (P<0.005) alleles in lichen planus patients, which indicated that these alleles might be risk factors and ‎increase the ability of infection. The present study indicates that genetic constitution through HLA-DQ locus determines ‎the mechanism of disease as well as clinical and pathologic outcomes. More studies are necessary to test genetic ‎dependencies on the basis of larger samples which would increase statistical power. An accurate definition of disease ‎susceptible alleles will improve our understanding of antigen presentation mechanisms prevailing in the etiology of the ‎disease. This knowledge is necessary for the design of improved immune intervention strategies to halt lichen planus ‎progression in patients at risk of developing the disease or those who are already suffering from it.‎