title: Low erythrocyte complement receptor type 1 (CR1, CD35) expression in preeclamptic gestations.
abstract: OBJECTIVE
  Erythrocyte complement receptor type 1 (E-CR1) is the main immune complex clearance mechanism in humans. Decreased E-CR1 expression is noted in certain inflammatory disorders. Recent evidence implicates inflammation in the pathogenesis of preeclampsia. We investigated whether E-CR1 is decreased in preeclampsia.
  
  
  METHODS
  E-CR1 protein expression was quantified by radioimmunoassay. Plasma concentration of soluble CR1 was quantified using a specific enzyme linked immunosorbent assay. Quantitative genotypes were evaluated by HindIII restriction fragment length polymorphism analysis.
  
  
  RESULTS
  E-CR1 expression was reduced in patients with preeclampsia. Lack of neoantigen expression (indicative of enzymatic cleavage of CR1) or elevated plasma-soluble CR1 was evidence against an acquired loss of E-CR1. Genotype analysis revealed a higher frequency of a CR1 allele associated with low E-CR1 expression in preeclampsia when compared with normal pregnant controls.
  
  
  CONCLUSIONS
  E-CR1 expression is decreased in preeclamptic patients and levels correlate with severity of disease. This condition may have a genetic basis in some patients.
authors.affiliation: Department of Obstetrics, Gynecology and Reproductive Biology, Brigham and Women's Hospital, Boston, MA, USA. bfeinberg@sbhcs.com
authors.forename: Bruce B
authors.initials: BB
authors.lastname: Feinberg
authors.forename: Richard M
authors.initials: RM
authors.lastname: Jack
authors.forename: Samuel C
authors.initials: SC
authors.lastname: Mok
authors.forename: Deborah J
authors.initials: DJ
authors.lastname: Anderson
mesh_terms: D004912:Erythrocytes / Q000276:immunology* / Q000378:metabolism; D005260:Female; D006801:Humans; D010447:Peptide Hydrolases / Q000276:immunology / Q000494:pharmacology; D012150:Polymorphism, Restriction Fragment Length; D011225:Pre-Eclampsia / Q000097:blood / Q000175:diagnosis*; D011247:Pregnancy; D017463:Receptors, Complement 3b / Q000096:biosynthesis* / Q000172:deficiency / Q000235:genetics
chemical_list: D017463:Receptors, Complement 3b; D010447:Peptide Hydrolases