Abstract
Recurrent miscarriages affect up to 5% of couples. CD3+ (T-lymphocytes), CD4+ (helper T-lymphocytes), CD8+ (cytotoxic T-lymphocytes), and CD20+ (B-lymphocytes) cells may participate in the pathophysiology of recurrent pregnancy loss (RPL). The aim of this study was to investigate the complicity of these molecules in RPL. The experimental specimens were obtained from 20 females who underwent miscarriages in the first gestational trimester, while the control group’s specimens consisted of 20 females who proceeded with voluntary pregnancy termination during the same period. Tissue samples were taken from the decidua basalis, decidua parietalis, and trophoblast (placental chorionic villi) and were studied using immunohistochemical methods. Monoclonal antibodies were used against CD3, CD4, CD8, and CD20 cells. The lymphocyte levels in the decidua parietalis displayed profound disparities among the two groups. The decidua basalis and trophoblast exhibited almost the same disparities regarding positive CD cells. The comparison of CD4+ and CD8+ cells in the endometrial tissue revealed a significant difference between the two groups of study. The analysis uncovered a strong relationship between RPL and the presence of CD3+, CD4+, CD8+, and CD20+ cells in the decidua parietalis tissue. The number of positive T cells was decreased in the decidual basalis and chorionic villi, proving that their absence significantly disrupts the balance of the immunological environment.
Highlights
Recurrent pregnancy loss (RPL) is described as the occurrence of two or three repeated abortions, prior to the 20th week of pregnancy [1]
The present experiment made an attempt to correlate the imbalance of CD3, CD4, CD8, and CD20 levels, and the dysregulation of the immune system in the endometrial tissue, with the RPL pathogenesis [15,16]
This study provides a comprehensive comparison of the CD3+, CD4+, CD8+, and CD20+ levels, in the decidua
Summary
Recurrent pregnancy loss (RPL) is described as the occurrence of two or three repeated abortions, prior to the 20th week of pregnancy [1]. There are numerous risk factors, mainly metabolic and anatomic, accompanied by systematic abnormalities and infections [2,3] To this date, even though there are a plethora of studies regarding the etiologic factors of RPL, the full comprehension of the immune dysregulation that causes miscarriages seems to be elusive [4]. Leukocytes are a significant component of the human endometrium of the female reproductive system. Their numbers increase to 10% of stromal cells, in the proliferative phase. The proportion of leukocytes increases to 30% of the decidual cells [5]. This indicates their implication in RPL [6–9]
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