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Updated: Jun 5, 2026

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Published on: May 19, 2020
The Cromer blood group system: a review
J R Storry1, M E Reid, M H Yazer
1Special Serology, Department of Clinical Immunology and Transfusion Medicine, University and Regional Laboratories, Division of Haematology and Transfusion Medicine, Department of Laboratory Medicine, Lund University, Lund, Sweden.
The Cromer blood group system antigens are on decay-accelerating factor (DAF). While rare, anti-Cromer antibodies can cause transfusion issues, but not hemolytic disease of the newborn due to placental DAF.
Area of Science:
- Immunology
- Hematology
- Genetics
Background:
- The Cromer blood group system antigens are located on decay-accelerating factor (DAF), a protein in the regulators of complement activation family.
- This system comprises 12 high-prevalence and three low-prevalence antigens, with known molecular underpinnings.
- Most antigens result from single nucleotide changes in the DAF gene, localized to specific complement control protein (CCP) domains.
Purpose of the Study:
- To review the characteristics of the Cromer blood group system.
- To discuss the molecular basis and clinical significance of Cromer antigens and associated antibodies.
Main Methods:
- Literature review of studies on Cromer blood group system antigens and decay-accelerating factor (DAF).
- Analysis of the genetic basis and protein localization of Cromer antigens.
- Examination of clinical implications, including transfusion reactions and hemolytic disease of the newborn (HDN).
Main Results:
- Individuals with the Cromer null phenotype (Inab) lack DAF but show no increased hemolysis susceptibility.
- Antibodies to Cromer antigens are infrequent but can lead to accelerated destruction of transfused red blood cells (RBCs).
- No risk of HDN is associated with Cromer system antibodies due to abundant fetally derived DAF in the placenta.
Conclusions:
- The Cromer blood group system, based on DAF, has well-defined antigens with specific genetic origins.
- While anti-Cromer antibodies pose a transfusion risk, they do not cause HDN, highlighting the protective role of placental DAF.
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