Paternal Leukocytes Selectively Increase Secretion of IL-4 in Peripheral Blood During Normal Pregnancies: Demonstrated by a Novel One-Way MLC Measuring Cytokine Secretion
Article first published online: 6 SEP 2011
American Journal of Reproductive Immunology
Volume 38, Issue 5, pages 320–326, November 1997
How to Cite
Ekerfelt, C., Ernerudh, J., Matthiesen, L. and Berg, G. (1997), Paternal Leukocytes Selectively Increase Secretion of IL-4 in Peripheral Blood During Normal Pregnancies: Demonstrated by a Novel One-Way MLC Measuring Cytokine Secretion. American Journal of Reproductive Immunology, 38: 320–326. doi: 10.1111/j.1600-0897.1997.tb00307.x
- Issue published online: 6 SEP 2011
- Article first published online: 6 SEP 2011
- Accepted April 30, 1997
- T cells
PROBLEM: It has been proposed that immune responses in normal pregnancy are Th2-like, thereby protecting the fetus and placenta from being rejected. Some studies have shown Th2-deviated systemic responses to different antigens and mitogens. The aim of this study was to demonstrate the specific T cell cytokine responses directed toward paternal histocompatibility leukocyte antigen (HLA), because this is the most prominent target for rejection of the feto-placental unit.
METHOD OF STUDY: A novel one-way mixed leukocyte culture (MLC) combined with the detection of cytokine secretion with a sensitive ELISPOT assay was developed. Peripheral blood from 11 pregnant women was investigated with respect to allo-reactivity toward paternal leukocytes and pooled leukocytes from unrelated blood donors. This was done at three different occasions during pregnancy and 8 weeks after delivery. Nine age-matched non-pregnant women served as controls.
RESULTS: In the second and third trimesters of pregnancy significantly larger numbers of IL-4-secreting cells (Th2) were induced by paternal leukocytes as compared to unrelated leukocytes.
CONCLUSIONS: The findings indicate a selective immune deviation toward Th2, which may protect the fetus from rejection and thus may be an important homeostatic mechanism in normal pregnancies.