Recent advances in cutaneous lupus.

Autor: Maz MP; Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, 48109, USA; Program in Immunology, University of Michigan, Ann Arbor, MI, 48109, USA., Martens JWS; Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, 48109, USA; Program in Immunology, University of Michigan, Ann Arbor, MI, 48109, USA., Hannoudi A; Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, 48109, USA., Reddy AL; Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, 48109, USA., Hile GA; Department of Dermatology, University of Michigan, Ann Arbor, MI, 48109, USA., Kahlenberg JM; Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, 48109, USA; Department of Dermatology, University of Michigan, Ann Arbor, MI, 48109, USA. Electronic address: mkahlenb@med.umich.edu.
Jazyk: angličtina
Zdroj: Journal of autoimmunity [J Autoimmun] 2022 Oct; Vol. 132, pp. 102865. Date of Electronic Publication: 2022 Jul 17.
DOI: 10.1016/j.jaut.2022.102865
Abstrakt: Cutaneous lupus erythematosus (CLE) is an inflammatory and autoimmune skin condition that affects patients with systemic lupus erythematosus (SLE) and exists as an isolated entity without associated SLE. Flares of CLE, often triggered by exposure to ultraviolet (UV) light result in lost productivity and poor quality of life for patients and can be associated with trigger of systemic inflammation. In the past 10 years, the knowledge of CLE etiopathogenesis has grown, leading to promising targets for better therapies. Development of lesions likely begins in a pro-inflammatory epidermis, conditioned by excess type I interferon (IFN) production to undergo increased cell death and inflammatory cytokine production after UV light exposure. The reasons for this inflammatory predisposition are not well-understood, but may be an early event, as ANA + patients without criteria for autoimmune disease exhibit similar (although less robust) findings. Non-lesional skin of SLE patients also exhibits increased innate immune cell infiltration, conditioned by excess IFNs to release pro-inflammatory cytokines, and potentially increase activation of the adaptive immune system. Plasmacytoid dendritic cells are also found in non-lesional skin and may contribute to type I IFN production, although this finding is now being questioned by new data. Once the inflammatory cycle begins, lesional infiltration by numerous other cell populations ensues, including IFN-educated T cells. The heterogeneity amongst lesional CLE subtypes isn't fully understood, but B cells appear to discriminate discoid lupus erythematosus from other subtypes. Continued discovery will provide novel targets for additional therapeutic pursuits. This review will comprehensively discuss the contributions of tissue-specific and immune cell populations to the initiation and propagation of disease.
Competing Interests: Declaration of competing interest JMK has received Grant support from Q32 Bio, Celgene/BMS, Ventus Therapeutics, Rome Therapeutics. and Janssen. JMK has served on advisory boards for AstraZeneca, Eli Lilly, EMD-Serano, GlaxoSmithKline, Gilead, Bristol Myers Squibb, Avion Pharmaceuticals, Provention Bio, Aurinia Pharmaceuticals, Ventus Therapeutics, and Boehringer Ingelheim. All other authors have nothing to disclose. All other authors have nothing to disclose.
(Copyright © 2022 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
Externí odkaz: