Abstract

We compared the presence of diverse cytokines and regulatory T and B cells in skin biopsies of discoid lupus erythematosus (DLE) and subacute cutaneous lupus erythematosus (SCLE). We included 19 patients with DLE, 13 with SCLE, 8 healthy controls, and 5 patients with hypertrophic scars. We assessed the CLASI activity score. To determine IL-22-producing cells and the subpopulation of CD4+/IL-17A+-, CD4+/IL-4+-, and CD4+/IFN-γ +-expressing T cells, CD123+/IDO+ pDCs, CD25+/Foxp3+ Tregs, and CD20+/IL-10+-producing B cells, an immunostaining procedure was performed. Also intracellular IL-22, IL-17, IL-4, IFN-γ, and Foxp3 in CD4 T cells, IL-10 in B cells, and IDO in pDCs were analyzed by flow cytometry in peripheral blood. The main cellular participation in both lupus groups was IL-17- and IL-22-producing cell responses both at skin and at peripheral blood but prevailed in DLE. The CLASI activity scores negatively correlated with Th22 subpopulation and positively correlated with CD25+/Foxp3+ Treg cells. In conclusion a proinflammatory and regulatory imbalance coexists in cutaneous lupus, both responses being more intense in DLE.

Highlights

  • Cutaneous lupus erythematosus is a chronic autoimmune disease with a broad spectrum of cutaneous manifestations that may precede systemic lupus erythematosus (SLE), stay as the only lupus feature, or occur at any stage of the disease among patients with SLE [1]

  • Diverse mechanisms have been implicated in the physiopathogenesis of cutaneous lupus erythematosus such as environmental factors, keratinocyte apoptosis, genetic susceptibility, B cell hyperactivity, the interaction of the innate and cell-mediated immunity, cytokine and chemokine release, and uncontrolled and persistent effector T cell responses that can drive the onset of skin lesions [3]

  • erythrocyte sedimentation rate (ESR) levels, cutaneous activity score, antidsDNA antibody levels, dose of prednisone, and antimalarials were conspicuously higher in subacute cutaneous lupus erythematosus (SCLE) compared with discoid lupus erythematosus (DLE) patients

Read more

Summary

Introduction

Cutaneous lupus erythematosus is a chronic autoimmune disease with a broad spectrum of cutaneous manifestations that may precede systemic lupus erythematosus (SLE), stay as the only lupus feature, or occur at any stage of the disease among patients with SLE [1]. CLE-specific lesions are further divided in acute (ACLE), subacute (SCLE), and chronic (CCLE) varieties; this last category includes the discoid lupus erythematosus (DLE) [2]. Cutaneous manifestations are heterogeneous and often represent a clinical challenge, which in turn reflects the complexity of the underlying pathogenic mechanisms. In this sense, diverse mechanisms have been implicated in the physiopathogenesis of cutaneous lupus erythematosus such as environmental factors (ultraviolet light exposure, drugs, etc.), keratinocyte apoptosis, genetic susceptibility, B cell hyperactivity, the interaction of the innate and cell-mediated immunity, cytokine and chemokine release, and uncontrolled and persistent effector T cell responses that can drive the onset of skin lesions [3]

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call