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Gestation stage-dependent mechanisms of invariant natural killer T cell-mediated pregnancy loss

Jonathan E Boyson1, Nisha Nagarkatti, Leena Nizam

  • 1Division of Transplantation Surgery and Immunology, Department of Surgery, University of Vermont College of Medicine, Burlington, VT 05405, USA.

Proceedings of the National Academy of Sciences of the United States of America
|March 16, 2006
PubMed

Stimulation of CD1d-restricted semiinvariant natural killer T cells by using the CD1d ligand alpha-galactosylceramide (alphaGalCer) induces pregnancy loss in mice through an ill-defined mechanism involving TNF, IFN-gamma, and perforin. In this article, we demonstrate that during early gestation, alphaGalCer efficiently induced pregnancy loss in C57BL/6J and BALB/cJ mice in a perforin-dependent manner. In contrast, during midgestation perforin was no longer required for pregnancy loss. Concomitant with the loss of a perforin requirement at midgestation was the emergence of strain-dependent variations in susceptibility to alphaGalCer-induced pregnancy loss. Whereas pregnant C57BL/6J mice remained susceptible to alphaGalCer at midgestation, pregnant BALB/cJ mice were resistant to its effects. Pregnancy loss during midgestation was correlated with dramatically higher serum cytokine levels, including TNF and IL-2, in the susceptible C57BL/6J strain compared with the resistant BALB/cJ strain. Thus, the stage of gestation defined two distinct mechanisms of pregnancy loss: a perforin-dependent mechanism operating at early gestation and a perforin-independent, cytokine-dominated mechanism operating after midgestation.

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