Characterization of autoantibodies and cytokines related to cutaneous lupus erythematosus

Abstract

Objective To investigate the profiles of anti-RPLP0, anti-galectin3 antibodies, interferon-α (IFN-α), interferon-λ1(IFN-λ1) and interleukin-17A/F(IL-17A/F) in the subtypes of cutaneous lupus erythematosus (CLE) including acute CLE (ACLE), subacute CLE (SCLE) and discoid lupus erythematosus (DLE). Methods Serum levels of autoantibodies and cytokines were determined by enzyme-linked immunoabsorbent assay (ELISA). Lupus lesions were evaluated by cutaneous lupus erythematosus disease area and severity index (CLASI). Results Serum anti-RPLP0, anti-galectin3 antibodies and IFN-λ1 were higher in systemic lupus erythematosus (SLE) patients with skin lesions than those without skin lesions, compared to healthy controls. IFN-α, IL-17A and IL-17F was elevated in all patients regardless of skin lesions. The two antibodies, IFN-α and IL-17A were positively correlated with the CLASI score in all patients with CLE. In addition, serum IL-17A was positively correlated to the CLASI score of ACLE, SCLE and DLE, while anti-RPLP0 and anti-galectin3 antibodies were only correlated to the score of SCLE and IL-17F to DLE. Conclusion Serum anti-RPLP0, anti-galectin3 antibodies, IFN-α, IFN-λ1 and IL-17A/F are associated with the occurrence of lupus skin lesions regardless of the systemic complications, whereas the profiles of these inflammatory mediators vary with the subtypes of lupus skin lesions.

Cytokines as Biomarkers in Systemic Lupus Erythematosus: Value for Diagnosis and Drug Therapy

“…Interestingly, besides IL-17, Th-17 cells also produce IFN- λ1, and together these molecules provide protection from pathogens on the skin surface [ 77 ]. Several studies reported that the majority of SLE patients have increased levels of IL-17A and IL-17F [ 78 , 79 ].…”

“…Levels of circulating IL-17A have been found to correlate with the Cutaneous Lupus Erythematosus activity and damage score index (CLASI) score [ 79 ], and high IL-17A expression has been demonstrated in the cellular infiltrates of the skin tissue of CLE lesions [ 80 ], as well as in kidneys affected by lupus nephritis (LN) [ 48 ]. High IL-17A levels at baseline predicted poor response to LN therapy [ 78 ] and deteriorating kidney function, if paralleled by INF-λ1 and IL-23 [ 18 ].…”

Regulation of B Cell Responses in SLE by Three Classes of Interferons

“…IFNλ was expressed in barrier tissues, making it a crucial mediator of SLE-associated skin inflammation. Surprisingly, IFNλ was also involved in autoimmune inflammation at non-barrier sites, including the joints and kidneys [ 102 , 108 , 111 ]. These data suggest a potential role for T3IFN signaling in the development of B cell-driven autoimmunity, although the direct role of T3IFN signaling in autoimmune B cell responses in SLE remains poorly understood.…”