The pathogenesis of cutaneous lupus erythematosus: The aberrant distribution and function of different cell types in skin lesions

Abstract

Lupus erythematosus (LE) is an autoimmune disease with diverse and complicated aetiology, including systemic lupus erythematosus (SLE) and cutaneous lupus erythematosus (CLE). CLE is a common manifestation of SLE, resulting in disfiguring scars, permanent hair loss and significant loss of quality of life for patients. 1 According to Gilliam and Sontheimer, CLE can be subdivided into three categories: acute cutaneous lupus erythematosus (ACLE), subacute cutaneous lupus erythematosus (SCLE) and chronic cutaneous lupus erythematosus (CCLE). 2 ACLE is often associated with systemic symptoms. 3 Half of SCLE patients meet criteria for SLE, though both of ACLE and SCLE often have mild SLE symptoms. 2 CCLE includes five different forms: discoid LE (DLE), verrucous/hypertrophic LE, LE profundus/panniculitis (LEP), LE tumidus (LET) and chilblain LE (CHLE). 3 DLE is the most

Immunomodulatory Role of the Antimicrobial LL-37 Peptide in Autoimmune Diseases and Viral Infections

“…These Abs bind self-nucleic acids released by dying cells and form immune complexes that are deposited in different parts of the body, leading to detrimental inflammation and tissue damage [51,52]. CLE usually presents as one of manifestations of SLE patients; however there are also a proportion of SLE patients present without cutaneous manifestations [53]. The skin is the primarily affected organ in CLE, where it is peculiarly photosensitive to UV light, which can induce new skin lesions and exacerbate existing CLE disease.…”

Interferon and interferon-induced cytokines as markers of impending clinical progression in ANA+ individuals without a systemic autoimmune rheumatic disease diagnosis

“…While it is possible that the serum levels of IFN-γ do not accurately reflect those produced in the tissues, there is some evidence that other IFNs can act coordinately with IFN-α to induce these cytokines. For example, in the skin, keratinocytes produce CXCL-10 in response to IFN-α [30]. SLE patients and some ANA + individuals lacking a SARD diagnosis have increased levels of IFN-κ in their skin [31], which amplifies the IFN-α response [32].…”

Efficacy of upadacitinib in a case of resistant lupus erythematosus tumidus

“…1 The exact pathogenesis of LET is not fully understood but Th1-biased inflammation mediated by Type I IFNs appears to play a significant role. 2 In CLE, the involvement of Th17 pathway is still under investigation although increased concentrations of IL-12 and IL-23 have been reported in SLE. 3 Moreover, some case reports have explored the use of anti-IL-17 and anti-IL-23 agents in different forms of CLE, including LTE, indicating their potential therapeutic utility.…”