Increased Prevalence of IL-17-Producing Peripheral Blood Lymphocytes in Pre-eclampsia
Article first published online: 10 FEB 2011
© 2011 John Wiley & Sons A/S
American Journal of Reproductive Immunology
Volume 66, Issue 3, pages 223–229, September 2011
How to Cite
Toldi, G., Rigó, J., Stenczer, B., Vásárhelyi, B. and Molvarec, A. (2011), Increased Prevalence of IL-17-Producing Peripheral Blood Lymphocytes in Pre-eclampsia. American Journal of Reproductive Immunology, 66: 223–229. doi: 10.1111/j.1600-0897.2011.00987.x
- Issue published online: 5 AUG 2011
- Article first published online: 10 FEB 2011
- Submitted September 19, 2010; accepted January 14, 2011.
Citation Toldi G, Rigó J Jr, Stenczer B, Vásárhelyi B, Molvarec A. Increased prevalence of IL-17-producing peripheral blood lymphocytes in pre-eclampsia. Am J Reprod Immunol 2011; 66: 223–229
Problem Systemic inflammation is a dominant component in the pathogenesis of pre-eclampsia. Besides the imbalance of Th1 and Th2 cells, alterations of the prevalence of Th17 and regulatory T cells have also been suggested to contribute to inflammation. We aimed to describe the prevalence of these four CD4 lymphocyte subtypes in pre-eclampsia and normal pregnancy, along with that of IL-17-producing CD8 and NK cells.
Method of study Twenty pre-eclamptic and 22 normal pregnant women were enrolled in this study. Using flow cytometry, we determined the prevalence of IL-17-producing cells among the CD4, CD8 and NK cell subsets. Furthermore, we measured the prevalence of CD4+ Tregs, and Th1/Th2 cells were characterized using cell surface chemokine receptor markers.
Results We demonstrated that there is a shift not only in the Th1/Th2 but also in the Th17/Treg balance favouring skewness towards a pro-inflammatory status in pre-eclampsia. The proportion of CD8 and NK cells that express IL-17 was also higher in pre-eclampsia.
Conclusion The prevalence of IL-17-producing CD4, CD8 and NK cells is elevated in pre-eclampsia, indicating that both the innate and adaptive arms of the immune system are involved in the development of the exaggerated maternal systemic inflammation observed in this pregnancy-specific disorder.