The role of the fetal immune system in the pathogenesis of RhD-hemolytic disease of newborns

Pavel Gurevich, Svetlana Erina, Sofia Gershon, Igor Zusman*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

9 Scopus citations

Abstract

Data in the literature and author's research regarding the role of the immune reaction of fetuses and newborns in the pathogenesis of RhD conflict and hemolytic disease of newborns was analyzed. In this disease, the immune response of fetuses and newborns is shown to develop under the effects of maternal antigens, including RhD IgG, which cross the placenta. One of the results is the formation of immune complexes (ICs) between the maternal antigens and fetal IgM. In the intensive immune reaction, these ICs are removed from the infants at a high rate. As a result, the intensity of erythrocyte destruction, the degree of anemia and hyperbilirubinemia decrease. Various forms of HDN are of different intrauterine duration: from a few days in the icteric form without anemia to a month or more, in the hydropic form. In the latter form, decompensation of the immune system develops; extravascular erythroclasia by macrophages is replaced by intravascular lysis of erythrocytes. We suggest some methods to determine the fetal condition and a cure for the most severe cases of HDN, as well as a way of decreasing RhD-sensitization in women. These suggestions may be of interest to specialists in pediatrics and obstetrics and may be of clinical use.

Original languageEnglish
Pages (from-to)76-89
Number of pages14
JournalHuman Antibodies
Volume8
Issue number2
DOIs
StatePublished - 1997

Keywords

  • Apoptosis
  • Erythroblastosis
  • Erythrophagocytosis
  • Fetal and neonatal diseases
  • Hemolysis
  • IgG
  • Immune complexes
  • Immunology
  • Pathogenesis
  • Pathology

Fingerprint

Dive into the research topics of 'The role of the fetal immune system in the pathogenesis of RhD-hemolytic disease of newborns'. Together they form a unique fingerprint.

Cite this