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Fertil Steril. 2005 Mar;83(3):598-605.

Role of the endometrial tripod interleukin-18, -15, and -12 in inadequate uterine receptivity in patients with a history of repeated in vitro fertilization-embryo transfer failure.

Author information

1
Institut National de Santé et Recherche Médicale (INSERM) U131, Equipe cytokines et relation materno-foetale, et Service de Gynécologie Obstétrique, Hôpital Antoine Béclère (AP-HP), Clamart, France. Ledeenathalie@aol.com

Abstract

OBJECTIVE:

To document in the endometrium the correlation among the interleukin (IL)-12, -15, and -18 mRNA and the correlation between cytokine levels, vascular status, and endometrial natural killer (NK) cell count in the context of recurrent implantation failure.

DESIGN:

A pilot study.

SETTING:

Department of Reproductive Immunology.

PATIENT(S):

Women who failed to become pregnant after repeated IVF-embryo transfer and fertile control subjects.

INTERVENTION(S):

Ultrasonic evaluation and endometrial biopsy in luteal phase.

MAIN OUTCOME MEASURE(S):

Uterine artery Doppler, count of uterine CD56 bright cells/field, and quantification by real-time polymerase chain reaction (PCR) to monitor IL-12 family (IL-12p40, IL-12p35, EBI3, IL-23), the IL-18 system (IL-18, IL-18R, IL18BP), and the IL-15 mRNA ratio.

RESULT(S):

The uterine artery Doppler and the CD56 bright cell counts were significantly different in fertile and infertile patients. The mean uterine artery pulsatility index correlated significantly negatively with the IL-18/actin ratio suggesting a defect of the cytokine-dependent vascular remodeling pathway. The number of uterine CD56 bright cells was significantly correlated with the IL-15/actin and IL-18/IL-18BP ratios. Thus, IL-18 and IL-15 seems to be involved in the local recruitment and the activation of uterine natural killer (uNK) cells. IL-18 was itself correlated with IL-15 and IL-12, suggesting a local control of uNK cells activation.

CONCLUSION(S):

The assessment of the tripod IL-12/-15/-18 shows distinct immune-related mechanisms that are involved in the broader context of inadequate uterine receptivity.

[Indexed for MEDLINE]

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