Killer cell immunoglobulin-like receptors (KIR) and human leukocyte antigen-C (HLA-C) allorecognition patterns in women with endometriosis

Abstract

chii-Ruey tzeng 1,2* endometriosis shares similarities with several autoimmune diseases. the human leukocyte antigen (HLA)-C genotype is associated with several human autoimmune diseases. HLA-c is a ligand of killer cell immunoglobulin receptors (KIRs) and is an essential regulator of natural killer cell activity, which is associated with endometriosis progression. polymorphisms in HLA-C and KIR affect the activity of NK cells and susceptibility to several diseases. Therefore, we attempted to investigate an association between HLA-C genotype and KIR polymorphism and the occurrence of endometriosis. We tested the association of certain KiR and HLA-c combinations and the development of endometriosis by characterizing both KIR and HLA-C genes in 147 women with endometriosis and 117 controls. The HLA-C genotypes and KIR polymorphisms were analyzed via DnA-based method for higher-resolution genotyping. We found that the occurrence of HLA-C*03:03*01 was increased in endometriosis than in control groups. Analysis of various KIR haplotypes revealed differences between the endometriosis and control cohorts. the number of KIR centromeric A/A haplotypes was increased in the endometriosis group than controls. Moreover, the endometriosis cohort was characterized by reduced number of KIR2DS2-positive individuals in the Han Chinese population. Our current findings suggest that the KIR and HLA-C genotypes are associated with the pathogenesis of endometriosis. Endometriosis is a chronic gynecological disease with unknown etiology and is characterized by extra-uterine growth of endometrial tissue 1. Endometriosis affects 6% to 10% of fertile women at the reproductive age and causes severe pelvic pain and infertility 2-4. Familial and twin studies have reported that genetic factors are associated with the pathogenesis of endometriosis 5-9. Cell-mediated and humoral immune responses are essential in the pathogenesis of endometriosis, since it is associated with various immunological abnormalities, particularly

A Brief Analysis of Tissue-Resident NK Cells in Pregnancy and Endometrial Diseases: The Importance of Pharmacologic Modulation

“…In aged mouse and humans, the resolution of endometriosis is delayed [34]. Chronic inflammation in endometrial tissue decreases the telomerase activity of several cells, impeding their optimal physiological response in mouse [34] and humans [21,[35][36][37][38][39]. trNK cells could also be affected by the low telomerase response [34].…”

“…trNK cells could also be affected by the low telomerase response [34]. On the other hand, senescent cells may activate the cytotoxic response of cNK cells [34][35][36][37][38][39] against autologous cells and, in consequence, generate more cell death maintaining the local chronic inflammatory response.…”

Lnc‐RNA LINC01279 induces endometriosis via targeting of HOXA10

“…As of now, pathogenesis of EMs remains unclear, but current evidence supports that EMs is correlated with an anomaly in uterus development. EMs is often the cause of infertility in women and treatment of EMs requires significant clinical tests and surgical treatment, with the administration of drugs that suppress the ovarian functions 5–10 . These drugs may harm the reproductive system and quality of life in women and often have a high incidence rate of postoperative complications.…”

“…These drugs may harm the reproductive system and quality of life in women and often have a high incidence rate of postoperative complications. Thus, it is imperative to explore effective targets in the treatment of EMs 5–10 …”

“…At the same time, the expression of HOXA10 gene fluctuated periodically under the influence of estrogen and progesterone, and the expression level reached its peak during the window period of fertilized egg implantation 16 . Besides its effect on uterus development, HOXA10 also decides on the acceptance of mice to the transplanted uterus 11,12,5,17 . In recent research, researchers found that HOXA10 expression was significantly lower in EMs patients than in healthy subjects, and the expression level of endometrial HOXA10 gene was also significantly lower in infertile EMs patients than in fertile EMs patients 18,19 .…”