Decidual memory T‐cell subsets and memory T‐cell stimulatory cytokines in early‐ and late‐onset preeclampsia

PROBLEM: Preeclampsia is a major cause of fetal and maternal mortality and morbidity. Disturbed fetal‐maternal immune tolerance, and therewith memory T cells, might be involved in its etiology. This study aims to give insight into memory T‐cell populations and its associated cytokines in the decidual layers in early‐onset preeclampsia (EO‐PE) and late‐onset preeclampsia (LO‐PE). METHOD OF STUDY: Lymphocytes were isolated from the decidua parietalis and basalis from EO‐PE (n = 6), LO‐PE (n = 8) and healthy (n = 15) pregnancies. CD4(+) and CD8(+) central‐ (CCR7(+)), effector‐ (CCR7(−)), tissue resident‐ (CD103(+)), and regulatory‐ (Foxp3(+)) memory cell (CD45RO(+)) populations and their activation status (CD69(+)) were analyzed using flow cytometry. qRT‐PCR analysis was performed on decidua parietalis and basalis biopsies to detect mRNA expression of interferon‐gamma, interleukin‐1B, IL2, IL6, IL7, IL8, IL10, IL15, and IL23. RESULTS: CD4(+) central‐memory (CM) cell proportions were lower in the decidua parietalis in LO‐PE (P < .0001) and EO‐PE (P < .01) compared to healthy pregnancies. CD8(+) memory (P < .05) and CD8(+) CM (P < .01) cell proportions were also lower in the decidua parietalis in EO‐PE compared to healthy pregnancies. This was accompanied by higher IL15 (P < .05) and IL23 (P < .05) and lower IL7 (P < .05) mRNA expression in decidua basalis biopsies from EO‐PE compared to healthy pregnancies, analyzed by qPCR. CONCLUSION: In conclusion, decidual memory T‐cell proportions, their activation status, and associated cytokines are altered in preeclampsia and might therefore be involved in fetal‐maternal immune tolerance and the pathophysiology of preeclampsia.