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.