Hidradenitis suppurativa (HS) is a chronic inflammatory cutaneous disease of the hair follicle typically presenting recurrent, painful, and inflamed lesions on the inverse areas of the body. Although its pathogenesis remains unknown, the immune system appears to play a potential role. To date, two previous studies have not found any association between the Human Leukocyte Antigen system (HLA) and HS. In this study we analyzed the HLA-A, -B, -C; and DRB1, -DQA1, and –DQB1 allele distribution in 106 HS patients and 262 healthy controls from a Caucasian population in Cantabria (northern Spain). HLA-A*29 and B*50 were significantly more common in HS patients and A*30 and B*37 in controls, but these associations disappeared after statistical correction. DRB1*07, DQA1*02, and DQB1*02 were significantly more common in controls (p 0.026, p 0.0012, and p 0.0005, respectively) and the HLA allele DQB1*03:01 was significantly more common in HS patients (p 0.00007) after the Bonferroni correction. The DRB1*07~DQA1*02~DQB1*02 haplotype was significantly more common in controls (p < 0.0005). This is the first study showing an association between HLA-class II and HS. Our results suggest that HLA-II alleles (DRB1*07, DQA1*02, DQB1*02, and DQB1*03:01) and the DRB1*07~DQA1*02~DQB1*02 haplotype could influence resistance or susceptibility to HS.
Background:Hidradenitis suppurativa (HS) is a chronic inflammatory cutaneous disease affecting terminal hair follicles in apocrine glands bearing skin. The pathogenesis of HS remains unknown, although increasing evidence suggests that the immune system plays an important role. To date, two previous studies, did not find any association betweenHLAand HS.Objectives:Our aim was to analyze the association of HLA class II with HS in a Caucasian population from Cantabria (northern Spain).Methods:In this study we analyzed theHLA-A, -B, -C, DRB1, -DQA1 and –DQB1allele distribution in 106 HS patients and 262 age- and sex-matched controls from a Caucasian population of Cantabria (northern Spain).Results:HLA-A*29 andB*50 were significantly more frequent in HS patients andA*30 andB*37 in controls, but these associations disappeared after correction. On the other hand,DRB1*07,DQA1*02 andDQB1*02 were significantly more frequent in controls (p0.026,p0.0012 andp0.0005 respectively), and theHLAalleleDQB1*03:01 was significantly more frequent in HS patients (p0.00007) all of them after Bonferroni correction. Furthermore, theDRB1*07;DQA1*02;DQB1*02 haplotype was significantly more frequent in controls (p0.0005).Conclusion:This is the first study showing an association of HLA-class II with HS. Our results suggest that HLA-II alleles (DRB1*07,DQA1*02,DQB1*02 andDQB1*03:01) and theDRB1*07~DQA1*02~DQB1*02 haplotype could influence on resistance or susceptibility to HS.References:[1]González-López MA. J Am Acad Dermatol. 2016; Aug;75(2):329-35.[2]González-López MA. PLoS One. 2018 Jan 4;13(1).[3]Vilanova I. J Eur Acad Dermatol Venereol. 2018 May;32(5):820-824.[4]Durán-Vian C, et al. J Eur Acad Dermatol Venereol. 2019 Nov;33(11):2131-2136.Disclosure of Interests:Monica Calderón-Goercke: None declared, J. Gonzalo Ocejo-Vinyals: None declared, Miguel A González-Gay Grant/research support from: Pfizer, Abbvie, MSD, Speakers bureau: Pfizer, Abbvie, MSD, Marcelo A. Fernández-Viña: None declared, Juan Cantos-Mansilla: None declared, Iosune Vilanova: None declared, Ricardo Blanco Grant/research support from: AbbVie, MSD, and Roche, Speakers bureau: AbbVie, Pfizer, Roche, Bristol-Myers, Janssen, and MSD, Marcos González-López: None declared
Background:Hidradenitis suppurativa (HS) is a chronic, relapsing inflammatory cutaneous disease affecting terminal hair follicles in apocrine-gland bearing skin. The pathogenesis of HS is still unknown, although increasing evidence suggests that the immune system plays an important role. In order to study the role of innate immunity we analyzed several Toll Like Receptors (TLRs) functional single nucleotide polymorphisms (SNPs). To date, only one previous study focused about the role of TLR4 SNPs in HS showing no association with this disease.Objectives:The main goal of this study was to analyze the role of several TLRs functional SNPs in HS patients and healthy controls, in a Caucasian population from Cantabria (northern Spain).Methods:Through a case-control study, we analyzed the allele and genotype distribution of the SNPs in 106 patients with HS and 278 age and sex matched healthy control subjects for the following SNPs (TLR1 rs5743611 and rs4833095, TLR2 rs5743704 and rs5743708, TLR6 rs5743810, and TLR10 rs11096955, rs11096957 and rs4129009, by Real-Time PCR using a TaqMan assay.Results:We did not find any significant difference in the allelic distribution of the different SNPs between HS patients and controls. Regarding genotypes, only TLR10 rs11096955 (dominant, codominant and overdominant), rs11096957 (dominant, codominant and overdominant) and rs4129009 (codominant and overdominant) showed significant differences between HS patients and controls. However, no association was found when we analyzed the different TLR10 haplotypes.Conclusion:To the best of our knowledge, this is the first study showing an association of TLR10 SNPs with HS.References:[1]González-López MA. J Am Acad Dermatol. 2016; Aug;75(2):329-35.[2]González-López MA. PLoS One. 2018 Jan 4;13(1)[3]Vilanova I. J Eur Acad Dermatol Venereol. 2018 May;32(5):820-824.[4]Durán-Vian C, J Eur Acad Dermatol Venereol. 2019 Nov;33(11):2131-2136.Disclosure of Interests:Monica Calderón-Goercke: None declared, J. Gonzalo Ocejo-Vinyals: None declared, Juan Irure-Ventura: None declared, María Gutiérrez-Larrañaga: None declared, Miguel A González-Gay Grant/research support from: Pfizer, Abbvie, MSD, Speakers bureau: Pfizer, Abbvie, MSD, Iosune Vilanova: None declared, Juan Cantos-Mansilla: None declared, Ricardo Blanco Grant/research support from: AbbVie, MSD, and Roche, Speakers bureau: AbbVie, Pfizer, Roche, Bristol-Myers, Janssen, and MSD, Marcos González-López: None declared
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