Lichen Planopilaris is Associated with HLA DRB1*11 and DQB1*03 Alleles

Abstract

There are no studies of the possible association of the human leukocyte antigen (HLA) system with lichen planopilaris (LPP). To determine whether the HLA system is associated with LPP, 40 consecutive Jewish Israeli patients with LPP (study group) and 252 volunteers (controls) were typed for DRB1*and DQB1* loci by molecular methods. Compared with controls, the study group had a significantly higher frequency of the DRB1*11 allele (62% vs. 21%, corrected p-value (pc) = 0.001) owing to increased frequencies of DRB1*11: 01 and DRB1*11: 04. The DQB1*03 allele was also expressed at a significantly higher frequency in the study group (70% vs. 33%, pc = 0.0005); specifically, the frequency of DQB1*03: 01 was increased. The majority (82.5%) of the patients were of non-Ashkenazi origin. We conclude that LPP appears to be over-represented in non-Ashkenazi Jewish patients and is associated with an increased frequency of HLA DRB1*11 and DQB1*03 alleles. These findings suggest that immunogenetic factors play a role in LPP.

Lichen planopilaris in three generations: grandmother, mother, and daughter – a genetic link?

“…The possible genetic background of LPP has been elucidated; however, rare familial occurrence of the disease has been suggested to not support this hypothesis. 1 Herein we report a familial case of LPP that occurred at a young age in a daughter, mother, and grandmother.…”

“…Lichen planopilaris (LPP) is a follicular variant of lichen planus. The possible genetic background of LPP has been elucidated; however, rare familial occurrence of the disease has been suggested to not support this hypothesis …”

The potential role of HLA-DRB1*11 in the development and outcome of haematopoietic stem cell transplantation-associated thrombotic microangiopathy

“…The association of HLA-DRB1*11 was documented with certain autoimmune, infectious and malignant conditions such as systemic sclerosis, Henoch-Schönlein purpura, Helicobacter pylori-positive idiopathic thrombocytopenic purpura, hairy cell leukaemia, cervical cancer and others. [33][34][35][36][37][38][39][40][41][42] Interestingly, in hairy cell leukaemia, anti-CD22 recombinant immunotoxin BL22-induced haemolytic uraemic syndrome (another, not ADAMTS13 deficiency-associated form of TMA) was also associated with HLA-DRB1*11. 33 The wide clinical spectrum of HLA-DRB1*11-associated conditions advocate the co-occurrence of additional provoking factors, because a unique mechanism is unlikely to drive all the above mentioned conditions.…”

A proposed mechanism for central centrifugal cicatricial alopecia

“…Due to the possible genetic nature of CCCA, molecular typing of human leukocyte antigen (HLA) testing using sequence‐specific primers or oligonucleotides of patients affected with CCCA against controls , . These studies can elucidate and localize genetic areas of pertinence for CCCA, and perhaps other primary cicatricial alopecias or fibrotic diseases common to African‐Americans.…”

“…HLA testing in a Jewish population with LPP demonstrated an statistically significant increase in the frequency in the DRB1*11:01, DRB1*11:04 and DQB1*03:01 alleles compared to controls . This leads credence to a possible genetic basis for LPP.…”