SOCS3 expression in cutaneous lichen planus

Abstract

Abstract Background: Lichen Planus (LP) is an idiopathic, inflammatory, autoimmune disease. The aetiopathogenesis of LP is still unclear. Suppressor of cytokine signaling- 3 (SOCS3) is known to inhibit cytokine signaling through Janus kinase (JAK) /signal transducers, activators of transcription , NFkB, and focal adhesion kinase (FAK) signaling pathways. Modulation of SOCS3 level leads to immune dysfunction. Aim of the work: Our study aimed to detect a possible role of SOCS3 in cutaneous LP Methods: In this case - control study skin biopsies were collected from 30 LP patients and 30 healthy volunteers. Biopsies were kept in lysis solution frozen at -80 Celsius till analysis of SOCS3 using Real time polymerase chain technique (RT-PCR) was done. Results: The expression of SOCS3 in cutaneous LP was significantly higher when compared to normal skin from healthy controls (p < 0.001). Conclusion: SOCS3 might play a role in the pathogenesis of LP