Endometrial expression of T-cell immunoreceptor with Ig and ITIM domains and cluster of differentiation 155: A case-control study of a novel immunomodulatory axis in endometriosis

Abstract

Background: Endometriosis is a chronic inflammatory disorder affecting about 10 of females in their reproductive years, characterized by endometrial tissue growing outside the uterus. Immune checkpoints play a crucial role in regulating the immune system and preserving homeostasis. T-cell immunoreceptor with immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domains (TIGIT), a newly discovered immune checkpoint, interacts with its ligand, cluster of differentiation 155 (CD155), to exert inhibitory effects on immune responses. Objective: Though numerous studies have explored the immunological profile in endometriosis cases, limited information exists about the potential role of TIGIT/CD155 interaction. Materials and Methods: This case-control study aimed to investigate the expression levels of TIGIT and CD155 genes in ectopic and eutopic tissues of 20 women diagnosed with endometriosis by a gynecologist with laparoscopy compared to the endometrium of 20 women without endometriosis, using real-time polymerase chain reaction. Results: Results showed that both TIGIT and CD155 gene expressions were significantly higher in ectopic endometrial tissues (p < 0.0001). CD155 is also upregulated in the eutopic endometrium of cases (p < 0.0001). However, no significant difference in TIGIT expression was observed between eutopic endometrium of cases and controls (p = 0.49). Conclusion: These findings suggest an upregulation of the TIGIT/CD155 pathway in endometriosis, indicating its potential role in the disease's pathogenesis. Further research is necessary to fully understand this signaling pathway and explore its viability as a biomarker for diagnosis and immunotherapy.