Recent advances in cytokines in cutaneous and systemic lupus erythematosus

Abstract

Lupus erythematosus (LE) includes a broad spectrum of diseases from a cutaneous-limited type to a systemic type. Systemic lupus erythematosus (SLE) is a systemic autoimmune disease which affects multiple organs. Cutaneous lupus erythematosus (CLE) includes skin symptoms seen in SLE and cutaneous-limited LE. Although immune abnormalities, as well as heritable, hormonal and environmental factors, are involved in the pathology of LE, the actual pathogenesis is still unclear. Recently, the involvement of various cytokines has been shown in the pathogenesis of LE. Moreover, some trials with biological agents targeted specific cytokines are also ongoing for SLE. In this article, we review the contributions of major cytokines such as interferon, tumor necrosis factor-α and interleukin-18 to LE, especially SLE and CLE.

Apoptotic signal molecules in skin biopsies of cutaneous lupus erythematosus: analysis using tissue microarray

“…The Notch gene pathway is involved in the development of many vertebrate organ systems (1). Responses are effected through interactions between Notch receptors and their ligands, Delta and Jagged, and function as determinants of cell fate (2).…”

“…UV light) leading to an abnormal immune response that involves the production of autoantibodies and immune complexes (1)(2)(3)(4)(5). After UV irradiation, apoptotic cells accumulate in CLE lesions which might be due to increased apoptosis or impaired/delayed clearance of apoptotic cells (6,7).…”

Update on cutaneous lupus erythematosus

“…Interleukin (IL)-18 and the overexpression of IL-18 receptor in keratinocytes was found to induce the apoptosis of keratinocytes via increased tumor necrosis factor (TNF)-α and decreased IL-12 production. [4] This apoptotic death was reported to be due to the strong expression of TNF-related apoptosis-inducing ligand (TRAIL) in the skin and the blood of patients with CLE. [5] Some CLE lesions showed increased levels of IL-17, but the precise role of IL-17 is uncertain [4] Moreover, transforming growth factor (TGF)-β serum levels were found to be significantly lower in patients with DLE as compared to the levels in patients with psoriasis and in healthy controls.…”

“…[4] This apoptotic death was reported to be due to the strong expression of TNF-related apoptosis-inducing ligand (TRAIL) in the skin and the blood of patients with CLE. [5] Some CLE lesions showed increased levels of IL-17, but the precise role of IL-17 is uncertain [4] Moreover, transforming growth factor (TGF)-β serum levels were found to be significantly lower in patients with DLE as compared to the levels in patients with psoriasis and in healthy controls. This downregulation of TGF-β and IL-10 in DLE may lead to defective immune suppression and thus to the generation of the tissue injury that is found in lupus patients.…”

Cutaneous lupus erythematosus: updates on pathogenesis and associations with systemic lupus

“…The frequency of cutaneous manifestations in SLE is as high as 70% [1], and the overall prevalence of CLE is reported as greater than 0.07% [2] and may be equivalent to SLE in some populations[3]. Subtypes of CLE are currently grouped on the basis of histology, lesion duration, clinical findings, and laboratory abnormalities [4, 5] and are summarized in Table 1.…”