Exploring The Pathological Role Of Cd8/ Bcl2 Axis In Lichen Planus- A Cross- Sectional Study

Abstract

INTRODUCTION:-

Lichen planus (LP) is a chronic inflammatory autoimmune disorder that affects the skin, mucous membranes, nails, and hair. It is characterized by immune system dysfunction, where CD8+ T cells attack basal keratinocytes, leading to inflammation and tissue damage. LP presents in various forms, including classic skin lesions, oral ulcers, genital lesions, nail changes, and, in some cases, esophageal and ocular involvement. While the exact etiology is unclear, genetic predisposition, stress, and immune dysregulation are significant contributing factors. The Bcl2/CD8+ axis plays a crucial role in the survival of CD8+ T cells during inflammation, and dysregulation of this axis may contribute to the chronicity of LP. This study investigates the expression of the CD8/Bcl2 axis in LP’s pathological process, with the goal of identifying potential therapeutic targets for more effective management of the condition.

AIMS AND OBJECTIVES:

To evaluate the histopathological features and immunohistochemical expression of CD8+ T cells and Bcl-2 in lichen planus and lichenoid dermatitis.

To assess cytotoxic lymphocytes and apoptosis in tissue samples.

To explore the role of CD8+ T cells and Bcl-2 in the pathogenesis and chronicity of these conditions.

MATERIALS AND METHODS:

This cross-sectional study was conducted at the Central Laboratory, Department of Pathology, Sree Balaji Medical College, Chennai, from February to July 2024. A total of 23 lichen planus and 24 lichenoid dermatitis samples were analyzed for CD8+ T cells and Bcl-2 expression. Data were analyzed using SPSS v25, with descriptive statistics, Spearman’s rank correlation, and the Chi-square test. A p-value of < 0.05 was considered statistically significant.

RESULTS:
Our study revealed an equal gender distribution in patients with lichen planus (LP), consistent with previous studies. Lesions were most commonly found on the legs, thighs, and ankles. Histopathologically, we observed characteristic lymphocytic infiltration in the subepidermal dermis, along with weak or absent expression of Bcl-2 in basal keratinocytes. Additionally, corticosteroid and UVB treatments led to reduced Bcl-2 and CD8 expression in skin biopsies. Notably, five patients developed LP lesions following COVID-19 vaccination, aligning with prior reports of vaccines potentially triggering LP.

DISCUSSION:
Our findings support the idea that immune dysregulation, specifically involving CD8+ T cells and Bcl-2, plays a key role in the pathogenesis and chronicity of LP. The presence of high levels of IL-12, IL-6, IL-21, and other cytokines suggests that targeting the JAK1 receptor could offer therapeutic potential. The link between vaccinations and LP flare-ups warrants further investigation, as the Th1 immune response may contribute to the development of skin lesions.

CONCLUSION:
Lichen planus is an immune-mediated disorder driven by CD8+ T cell activity and apoptosis of basal keratinocytes. The reduced expression of Bcl-2 and the role of cytokines such as IL-12, IL-6, and IL-21 contribute to the disease's persistence. Vaccinations, including the COVID-19 vaccine, may trigger LP in some individuals. Further research is needed to better understand the pathogenesis and explore targeted therapies for managing LP more effectively.