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[The role of immune placental inflammation in the genesis of complicated pregnancy].

[Article in Russian]


Immune inflammation is a typical pathophysiological process caused by exogenous and endogenous factors. Fibrinoid necrosis and cell infiltrations are the morphological features of tissue lesion caused by immune inflammation. Tissue lesion in immune inflammation may be connected with immune complex (IC) formation or T-cell aggression. Lesion caused by antigen-antibody complexes develops as a result of direct IC formation in the tissue or their inflow from microcirculation. Potential sources of IC in the placenta are maternal blood flow, the formation of IC between maternal antibodies (AB) and embryonic antigens, and IC formation in fetal blood vessels. After sedimentation in the placenta, circulating IC can cross syncytiotrophoblast tissue with the participation of specific receptors to immunoglobulin Fc-fragment. The process of antifetal AB formation may start in the maternal organism, as a result of which it forms AB to embryonic and placental antigens, including paternal Rh, ABO, and HLA, and some trophoblast antigens. IC are able to initiate inflammatory process through interaction with the compliment system, through the activation of macrophages excreting cytokines (TNF-alpha and IL-1), and through influencing basophiles and thrombocytes (the liberation of vasoactive amines). Gestosis is associated with system inflammatory response with endothelial dysfunction as the main element. As the clinical features of gestosis do not develop before 20 weeks of pregnancy, its clinical manifestation is preceded by increased fetal blood-brain barrier permeability, elevation of the level of neurospecific proteins of fetal origin in maternal circulation, and the formation of specific IC causing acute endotheliosis.

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