An immunological insight into the origins of pre-eclampsia.
BACKGROUND
Pre-eclampsia is a syndrome of heterogeneous origin characterized by deficient placentation due to the inability of the cytotrophoblast to acquire an invasive phenotype and to remodel the uterine spiral arteries. One of the main problems observed early in pre-eclampsia is an altered regulation of the immune system, where the shift toward a Th2 cytokine profile observed in normal pregnancies, does not occur. In pre-eclampsia, high interferon (IFN)-gamma concentrations are present, along with transforming growth factor-beta cytokines, which retard migration of cytotrophoblasts.


METHODS
A review of the scientific literature was performed on the immunological factors associated with the origins of pre-eclampsia. The various components of the immune system that may be participating in the aberrant immune activation that pathologically affect early pregnancy events and inhibit cytotrophoblast invasion were identified.


CONCLUSIONS
Cells and their signaling and regulatory molecules have been implicated in the immunological alterations found in the placental microenvironment of patients who develop pre-eclampsia. One of the main differences found in pre-eclampsia is a shift toward Th1 responses and the production of IFN-gamma. The origin of IFN-gamma is not clearly identified and could be the uterine natural killer cells, the placental dendritic cells modulating Th responses, alterations in synthesis of or response to regulatory molecules, or changes in the function of regulatory T cells in pregnancy. Aberrant immune responses promoting pre-eclampsia may also be due to an altered fetal allorecognition or to inflammatory triggers. Understanding the immunological basis for pre-eclampsia will expand knowledge regarding other adverse pregnancy outcomes.
Laresgoiti-Servitje
Estibalitz
E
Department of Immunology, School of Health Sciences, Universidad Anáhuac, Mexico City, Mexico.
Gómez-López
Nardhy
N
Olson
David M
DM
D016207:Cytokines / Q000502:physiology; D003713:Dendritic Cells / Q000502:physiology; D005260:Female; D006801:Humans; D050503:Indoleamine-Pyrrole 2,3,-Dioxygenase / Q000502:physiology; D007371:Interferon-gamma / Q000502:physiology; D007694:Killer Cells, Natural / Q000502:physiology; D008285:Major Histocompatibility Complex / Q000502:physiology; D010929:Placentation / Q000276:immunology*; D011225:Pre-Eclampsia / Q000276:immunology*; D011247:Pregnancy; D011971:Receptors, Immunologic / Q000502:physiology; D050378:T-Lymphocytes, Regulatory / Q000502:physiology; D018417:Th1 Cells / Q000502:physiology; D018418:Th2 Cells / Q000502:physiology
D016207:Cytokines; D050503:Indoleamine-Pyrrole 2,3,-Dioxygenase; D011971:Receptors, Immunologic; D007371:Interferon-gamma