Abstract
Background Alopecia areata (AA) is an acquired hair loss disorder induced by a cell-mediated autoimmune attack against anagen hair follicles. CD27-CD70 is a receptor-ligand complex which enhances T helper and cytotoxic T cell activation, survival, and proliferation. The overstimulation of this complex can lead to a lack of tolerance and the development of autoimmunity. Objectives This study aimed to assess the gene expression of CD27 and CD70 in patients with AA. Methods CD70 and CD27 mRNA expressions were evaluated by a quantitative real-time polymerase chain reaction in scalp biopsies from 40 AA patients (both AA lesions and non-lesional areas) and 40 healthy controls (HCs). The Severity of Alopecia Tool (SALT) score was used to assess AA severity. Patients were evaluated for signs of AA activity, including a positive hair pull test and dermoscopic features of black dots, broken hairs, and tapering hairs. Results The gene expression of CD70 and CD27 was significantly higher in AA lesions than in non-lesional areas (p < 0.001 for both) and HCs (p=0.004, p=0.014, respectively). There were significant positive correlations between AA severity and gene expression of CD70 (p < 0.001) and CD27 (p=0.030) in AA lesions. Significant associations were detected between signs of AA activity and lesional gene expression of CD70 and CD27. Additionally, CD70 and CD27 gene expression was significantly lower in non-lesional biopsies compared to HCs (p < 0.001). Conclusion Gene expression of CD70 and CD27 was increased in AA lesions and was associated with disease severity and activity. Thus, both molecules can be a predictor of AA severity and activity. Furthermore, the expression was reduced in non-lesional scalp areas. Thus, a lack of CD27 and CD70 expression may initially predispose to immunological dysregulation and the development of AA.
Highlights
Alopecia areata (AA) is an acquired non-cicatricial hair loss disorder affecting 0.1%–0.2% of individuals worldwide [1]
CD70, the uniquely identified ligand of CD27, belongs to the tumor necrosis factor family and is expressed exclusively on activated T cells, B cells, natural killer cells, and dendritic cells. e expression of CD70 is triggered by T cell activation upon antigen receptor attachment, toll-like receptor, or CD40 signaling. e interaction between CD70 on stimulated antigen presenting cells (APCs) and CD27 on T cells generates costimulatory signals that enhance and cytotoxic T (cT) cell activation, survival, proliferation, chemotaxis, and Dermatology Research and Practice cytokine production such as interleukin 2 and interferon-c [5]
CD70 is merely expressed upon T cell activation, and blocking the C27-CD70 complex has been proposed as an appealing treatment target for autoimmune disorders [9]
Summary
Alopecia areata (AA) is an acquired non-cicatricial hair loss disorder affecting 0.1%–0.2% of individuals worldwide [1]. CD70, the uniquely identified ligand of CD27, belongs to the tumor necrosis factor family and is expressed exclusively on activated T cells, B cells, natural killer cells, and dendritic cells. E interaction between CD70 on stimulated antigen presenting cells (APCs) and CD27 on T cells generates costimulatory signals that enhance and cT cell activation, survival, proliferation, chemotaxis, and Dermatology Research and Practice cytokine production such as interleukin 2 and interferon-c [5]. CD70 is merely expressed upon T cell activation, and blocking the C27-CD70 complex has been proposed as an appealing treatment target for autoimmune disorders [9]. Alopecia areata (AA) is an acquired hair loss disorder induced by a cell-mediated autoimmune attack against anagen hair follicles. CD27-CD70 is a receptor-ligand complex which enhances T helper and cytotoxic T cell activation, survival, and proliferation. Results. e gene expression of CD70 and CD27 was significantly higher in AA lesions than in non-lesional areas (p < 0.001 for both) and HCs (p 0.004, p 0.014, respectively)
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