P-280 Influences of CD8(+) tissue resident memory T cells on eutopic endometrial immune microenvironment and endometrial receptivity of minimal/mild endometriosis

This is the authors' abstract. We don't add key points for this paper.

Study question Our study aimed to focused on the influence of CD8+ tissue resident memory T cells (CD8+ TRM) on endometrial immune microenvironment and endometrial receptivity. Summary answer CD8+TRM participated in inflammatory endometrial immune microenvironment, influenced expression of endometrial receptivity and decidualization markers of stromal cells of eutopic endometrium of minimal/mild endometriosis. What is known already CD8+ tissue resident memory T cells (CD8+ TRM) are abundant in endometrium,CD8+ TRM have important physiological functions and of pathological significance in endometrium. Study design, size, duration Endometrial samples were collected using Pipelle sampling from women with or without endometriosis (minimal/mild) during hysteroscopy-laparoscopy. Tissue for immunofluorescence was fixed in 4% paraformaldehyde, for cell analysis was isolated into single cell immediately. Participants/materials, setting, methods We analyzed number variation, tissue location, cytotoxicity, degranulation and cytokine secretion of CD8+TRM in endometriosis and control during menstrual cycle through flow cytometry and polychromatic tissue immunofluorescence. We cocultured CD8+TRM and endometrial stromal cell to know the influence of CD8+TRM to endometrial receptivity and decidualization. The concentration of TNF-α, IFN-γ, IGFBP-1 and PRL were analyzed via ELISA and q-PCR. Western blot and q-PCR were used to test the expression level of HOXA10 and FOXO1. Main results and the role of chance Flow cytometry founded that the number of CD8+TRM in proliferative phase were more than secretory phase in both endometriosis and control. CD8+TRM were not only scattered in stroma of endometria, and also gathered in lymphoid aggregates. During secretory phase, the cytotoxicity, degranulation, and inflammatory cytokine expression resourced from CD8+ TRM were higher in endometriosis than control. CD8+TRM inhibited the expression of endometrial receptivity markers (HOXA10 and FOXO1) and decidualization markers (IGFBP-1 and PRL) of endometrial stromal cells in coculture system. When blocking the IFN-γ in coculture system, the expression of endometrial receptivity markers and decidualization markers were improved. Limitations, reasons for caution The mechanism of CD8+TRM influence on endometrial receptivity and decidualization of endometriosis is needed to further investigation. Wider implications of the findings CD8+TRM participated in inflammatory endometrial immune microenvironment, influenced expression of endometrial receptivity and decidualization markers of stromal cells of eutopic endometrium of minimal/mild endometriosis. CD8+TRM and its secretion of IFN-γ could be immunotherapeutic target for defective endometrial receptivity of endometriosis. Trial registration number NA