Circulating and skin biopsy-present cytokines related to the pathogenesis of cutaneous lupus erythematosus |
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| Institution: | 1. Fundación Valle del Lili, Centro de Investigaciones Clínicas, Cra 98 No. 18-49, Cali 760032, Colombia;2. Southern Illinois University School of Medicine, Department of Medical Microbiology, Immunology and Cell Biology, Springfield, IL, USA;3. Universidad Icesi, CIRAT: Centro de Investigación en Reumatología, Autoinmunidad y Medicina Traslacional, Calle 18 No. 122-135, Cali, Colombia;4. Fundación Valle del Lili, Unidad de Reumatología, Cra 98 No. 18-49, Cali 760032, Colombia;1. Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan;2. Division of Rheumatology, Department of Internal Medicine, Fujita Health University School of Medicine, Aichi, Japan;3. Center for General Medicine Education, Keio University School of Medicine, Tokyo, Japan;4. Chugai Pharmaceutical Co. Ltd., Kanagawa, Japan;1. Rheumatology Department, Guy''s and St. Thomas'' Hospitals NHS Foundation Trust, London, UK;2. Lane Fox Respiratory Medicine Department, Guy''s and St. Thomas'' Hospitals NHS Foundation Trust, London, UK;3. Department of Medical Oncology, Guy''s and St. Thomas'' Hospitals NHS Foundation Trust, London, UK;1. Laboratory of Pathophysiological and Nutritional Biochemistry, Université Libre de Bruxelles, Belgium;2. Université Libre de Bruxelles (ULB), Hôpital Universitaire de Bruxelles (H.U.B), CUB Hôpital Erasme, Rheumatology Department, Route de Lennik, 808 1070 Brussels, Belgium;1. Department of Clinical Immunology and Rheumatology, Sanjay Gandhi Postgraduate Institute of Medical Sciences (SGPGIMS), Lucknow, India;2. School of Telemedicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences (SGPGIMS), Lucknow 226014, India;3. Unit of Immunology, Rheumatology, Allergy and Rare Diseases (UnIRAR), IRCCS San Raffaele Hospital, Vita-Salute San Raffaele University, 20132 Milan, Italy;4. Clinical Immunology and Rheumatology Services, Department of Internal Medicine, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh 160012, India;1. International School of Medicine, Istanbul Medipol University, Istanbul, Turkey;2. Laboratory for Industrial and Applied Mathematics (LIAM), Department of Mathematics and Statistics, York University, Toronto, Canada;1. Department of Rheumatology, The Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, China;2. Shanxi Key Laboratory of Immunomicroecology, Taiyuan, Shanxi, China;3. College of Basic Medicine, Shanxi Medical University, Taiyuan, Shanxi, China;4. Pathology, Joint Program in Transfusion Medicine, Brigham and Women’ Hospital/Children''s Hospital, Harvard Medical School, Boston, MA, USA |
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| Abstract: | Cutaneous lupus erythematosus (CLE) is a common disease that may appear as a separate entity from systemic lupus erythematosus (SLE), precede SLE development, or occur as a manifestation of this systemic disease. It has a complex pathophysiology that involves genetic, environmental, and immune-mediated factors creating a self-amplification pro-inflammatory cycle. CLE is characterized by prominent type I interferons (IFNs) inflammation which are considered as the first precursors of the inflammatory cascade generated within the pathophysiology of CLE. TNF-α enhances the production of antibodies through the activation of B cells, and favors the expression of surface nuclear antigens on keratinocytes. UV light exposure favors keratinocyte apoptosis or necroptosis, which results in the release of multiple proinflammatory cytokines, including IL-6, IL-1α, IL-1β, TNF-α, IFNs, and CXCL10. Serum levels of IL-17 are elevated in patients with ACLE, SCLE, and DLE. Evidence suggests IL-22 plays a role primarily in tissue repair rather than in inflammation. High expression of BAFF and its receptors have been found in lesioned keratinocytes of patients with CLE, and patients with CLE have lower serum levels of the regulatory cytokines TGF-β and IL-10. The chemokines CXCL9 and CXCL10 (CXCR3 ligands) have an increased expression among these patients, and their expression is correlated with IFNs levels. CXCR3 ligands recruit cytotoxic type I cells through this receptor, further supporting the death of keratinocytes via necroptosis with the subsequent release of eNAs perpetuating the inflammatory cycle. Interface dermatitis is characterized by the presence of CXCR3-positive lymphocytes. This review describes the leading cytokines and chemokines present in the circulation and skin that play a fundamental role in the pathogenesis of CLE. |
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