Follicular helper T lymphocytes in the endometria of patients with reproductive failure: Association with pregnancy outcomes and inflammatory status of the endometria

Problem The phenotypes and functions of B and CD4+ T‐helper cell subsets during chronic inflammation of the endometria remain largely unexplored. This study aimed to investigate the characteristics and functions of follicular helper T (Tfh) cells to understand the pathological mechanisms of chronic...

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Veröffentlicht in:American journal of reproductive immunology (1989) 2023-07, Vol.90 (1), p.e13708-n/a
Hauptverfasser: Tian, Ye, Zeng, Qunxiong, Cheng, Yanfei, Wang, Xiao‐Hui, Cao, Dandan, Yeung, William Shu‐Biu, Liu, Qingzhi, Duan, Yong‐Gang, Yao, Yuan‐Qing
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Sprache:eng
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Zusammenfassung:Problem The phenotypes and functions of B and CD4+ T‐helper cell subsets during chronic inflammation of the endometria remain largely unexplored. This study aimed to investigate the characteristics and functions of follicular helper T (Tfh) cells to understand the pathological mechanisms of chronic endometritis (CE). Method of study Eighty patients who underwent hysteroscopic and histopathological examinations for CE were divided into three groups—those with positive results for hysteroscopy and CD138 staining (DP), negative results for hysteroscopy but positive CD138 staining (SP), and negative results for hysteroscopy and CD138 staining (DN). The phenotypes of B cells and CD4+ T‐cell subsets were analyzed using flow cytometry. Results CD38+ and CD138+ cells were mainly expressed in the non‐leukocyte population of the endometria, and the endometrial CD19+CD138+ B cells were fewer than the CD3+CD138+ T cells. The percentage of Tfh cells increased with chronic inflammation in the endometria. Additionally, the elevated percentage of Tfh cells correlated with the number of miscarriages. Conclusions CD4+ T cells, particularly Tfh cells, may be critical in chronic endometrial inflammation and affect its microenvironment, thereby regulating endometrial receptivity, compared to B cells.
ISSN:1046-7408
1600-0897
DOI:10.1111/aji.13708