Lichen planus: altered AIM 2 and NLRP 1 expression in skin lesions and defective activation in peripheral blood mononuclear cells

• DOI: 10.1111/ced.13859
• Publication Date: 2018-12-14T21:31:47Z
• Authors: R. Domingues; A. J. Pietrobon; G. C. Carvalho; N. Z. Pereira; N. V. Pereira; M. N. Sotto; V. Aoki; A. J. S. Duarte; M. N. Sato
• Keywords: TLR7

Lichen planus (LP) is an inflammatory skin disease with unknown aetiology. Activation by pathogen‐associated molecular patterns or environmental stimuli may activate some components of inflammasomes that contribute to the process in LP lesions. To characterize lesions and peripheral blood mononuclear cells (PBMCs) patients under Toll‐like receptor (TLR) activation. In total, 15 14 healthy controls (HCs) were enrolled study. Inflammasome expression was evaluated real‐time PCR immunohistochemistry, while ELISA used assess production interleukin (IL)‐1β PBMCs stimulation TLR4 TLR7/TLR8 agonists adenosine triphosphate (ATP). Compared levels HC samples, increased inflammasome AIM2 verified both epidermal dermal sections lesions, whereas NLRP1 IL‐β enhanced dermis. lesion samples exhibited higher transcript levels, similar lower pro‐IL‐1β mRNA compared samples. We that, from subjects, produced amounts IL‐1β after induction but agonists, regardless addition ATP. Alterations innate immunity, such as component PBMCs, observed LP. Further investigations dysfunctional activation chronic status are required.