PhD Scientific Days 2022

Clinical Medicine VII. (Poster discussion will take place in the Aula during the Coffee Break)

Immunohistochemical Study of the PD-1/PD-L1 Pathway in Cutaneous Lupus Erythematosus

Text of the abstract

Introduction
The pathomechanism of various autoimmune diseases is known to be associated with the altered function of programmed cell death 1/programmed cell death ligand 1 (PD-1/PD-L1) axis.
Aims
We aimed to investigate the role of this pathway and inflammatory cell markers in subtypes of cutaneous lupus erythematosus (CLE): discoid lupus erythematosus (DLE), subacute CLE (SCLE) and toxic epidermal necrolysis (TEN)-like lupus, a hyperacute form of acute CLE (ACLE).
Method
Ten skin biopsy samples from 9 patients were analysed with immunohistochemistry regarding the following markers: CD3, CD4, CD8, Granzyme B, CD123, CD163, PD-1, PD-L1. Our group consisted of 4 SCLE (2 idiopathic and 2 PD-1 inhibitor-induced), 4 DLE and 1 TEN-like lupus cases. From the latter patient, two consecutive biopsies were obtained 1 week apart. Marker expression patterns were compared through descriptive analysis.
Results
Higher median keratinocyte (KC) PD-L1 expression was observed in the SCLE group compared to the DLE group (65% and 5%, respectively). Medians of dermal CD4, Granzyme B, PD-1 positive cell numbers and GB+/CD8+ ratio were higher in the DLE group than in the SCLE group. The consecutive samples of the TEN-like lupus patient showed an increase by time in the number of infiltrating Granzyme B+ cytotoxic T-cells and KC PD-L1 expression (from 22 to 43 and 30% to 70%, respectively).
Conclusion
High KC PD-L1 expression might serve as a defence mechanism in acute skin reactions like TEN-like lupus and SCLE. In case of DLE low KC PD-L1 expression may contribute to the chronic course of the disease.
Funding
This work was supported by grants from the EFOP-3.6.3-VEKOP-16-2017-00009.