Association between the CCR5Δ32 polymorphism and preeclampsia

Background Preeclampsia (PE) is a condition that occurs in up to 7% of all pregnancies. Its exact pathophysiology is not known yet, but there is the involvement of genetic and immune factors maternal and fetal, with occurrence of hypertension and proteinuria. There is evidence of increased systemic inflammation during the first trimester of pregnancy in women with preeclampsia. The PE usually develops in the second half of pregnancy and is characterized by events of endothelial dysfunction and inflammation in its pathogenesis. Chemokines (proinflammatory cytokines) are considered the main determinants of the inflammatory response and its action by binding to specific receptors can be directly related to the development of PE. The chemokine receptor type 5 (CCR5) is a protein encoded by the CCR5 gene which is located on chromosome 3p21.3 p24. The polymorphic variant CCR5delta32 resulting from deletion of 32 base pairs in this gene leads to production of a nonfunctional isoform of the receptor, and has been implicated in a variety of autoimmune diseases.