Immunoactivation in preeclampsia: Vdelta2+ and regulatory T cells during the inflammatory stage of disease.
Recent data suggest a dominant role of the innate, rather than the adaptive immune system in pregnancy-related immunoregulation. gamma/delta T cells, that comprise a minor subpopulation of human peripheral blood lymphocytes, represent a link between the innate and the acquired immune systems. However little is known about how they function in preeclampsia, which is suggested to be associated with a Th1 predominant immune response. The aim of our study was to investigate the presence and phenotype of Vdelta2+ cells and of regulatory T cells in the pathogenesis of preeclampsia. Since Vdelta2+ T cell function has been shown to be altered in patients with preeclampsia we investigated the expression of perforin, Fas and TIM-3 by Vdelta2+ T cells and the possible role of activating and inhibitory NK cell receptors as well as of regulatory T cells. Vdelta2+ T cells of preeclamptic patients demonstrated an increased perforin and IFNgamma production, which could be explained by dysregulation of NK cell receptor expression. These Th1 polarized cells were less susceptible to apoptosis than Vdelta2+ T cells from healthy pregnant women. Our data suggest that activated Vdelta2+ T cells of preeclamptic women have an increased cytotoxic potential, which may be due to altered expression of NK cell inhibitory and activating receptors. In this study we report a series of observations, which taken together suggest the role of multiple pathways in generating an exaggerated systemic inflammatory response observed in the clinical stage of preeclampsia.
Miko
Eva
E
Department of Medical Microbiology and Immunology, University of Pecs, Medical School, Pecs, Hungary.
Szereday
Laszlo
L
Barakonyi
Aliz
A
Jarkovich
Andrea
A
Varga
Peter
P
Szekeres-Bartho
Julia
J
D000328:Adult; D017209:Apoptosis / Q000276:immunology; D018450:Disease Progression; D005260:Female; D005786:Gene Expression Regulation; D000072597:Hepatitis A Virus Cellular Receptor 2; D006801:Humans; D016130:Immunophenotyping; D007249:Inflammation; D007371:Interferon-gamma / Q000378:metabolism; D008213:Lymphocyte Activation; D008565:Membrane Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D055654:NK Cell Lectin-Like Receptor Subfamily C / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D054353:Perforin / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D011225:Pre-Eclampsia / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D011247:Pregnancy; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000276:immunology / Q000378:metabolism*; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D019014:fas Receptor / Q000235:genetics / Q000276:immunology / Q000378:metabolism
C448908:HAVCR2 protein, human; D000072597:Hepatitis A Virus Cellular Receptor 2; C527059:KLRC2 protein, human; D008565:Membrane Proteins; D055654:NK Cell Lectin-Like Receptor Subfamily C; D016692:Receptors, Antigen, T-Cell, gamma-delta; C521523:T-cell receptor Vdelta2, human; D019014:fas Receptor; D054353:Perforin; D007371:Interferon-gamma