Complete androgen insensitivity syndrome (CAIS), also known as Morris syndrome, is a rare X-linked recessive disorder characterized by a 46XY karyotype and a female external phenotype. We present the case of a 32-year-old patient who presented to Unimed International Hospital in 2024 with primary amenorrhea, infertility, and chronic pelvic pain. Clinical examination, imaging, and laboratory investigations led to the diagnosis of CAIS. Laparoscopic surgery was performed to remove bilateral gonadal structures and a cystic mass on the left side. Histopathological analysis revealed testicular tissue and a serous cystadenoma originating from the left mesonephric remnant. Following gonadectomy, hormone replacement therapy was initiated, resulting in stabilization of hormone levels. This rare case highlights the possibility of mesonephric remnant-derived cystadenoma in CAIS and underscores the diagnostic value of cytogenetic and histological evaluations, especially in distinguishing between ovarian and testicular tissue when imaging findings are inconclusive.

Introduction: When human body encounters external pathogens primary/innate immunity cells are activated by recognizing them and secondary/adaptive immunity is activated consecutively. Immune cell surface receptors, called Toll-like receptors (TLRs) recognize and bind pathogens. In our previous study, we revealed that there is a synergistic action between TLR9 and IFN-γ signaling in the endothelial cells. Purpose: To determine the role of negative and positive regulatory proteins on the IFN-γ/TLR9 synergistic signaling pathway Materials and Methods: This study was held in the Core Laboratory, Science Technology Center, Mongolian National University of Medical Sciences (MNUMS). In this study, murine endothelial cell (END-D) culture was used. The negative and positive regulator protein expression was detected by Western blotting. Result: Result of immunoblotting assay indicated that CpG DNA enhanced IFN-γ positive regulator protein p38 phosphorylation in the endothelial cells. Treatment by TLR9 ligand CpG DNA and IFN-γ increased p38 activation in 0.5 hour and 1 hour. CpG DNA inhibited IFN-γ negative regulator SOCS1 protein expression in 4 hr and 8 hr. Therefore, TLR9 ligand CpG DNA increased IFN-γ signal transduction in the endothelial cell line. Conclusion TLR9 ligand CpG DNA has decreased IFN-γ negative regulator protein SOCS1 expression. CpG DNA has increased IFN-γ positive regulator protein p38 phosphorylation.