PMID- 21175660
OWN - NLM
STAT- MEDLINE
DCOM- 20110412
LR  - 20171116
IS  - 1423-0410 (Electronic)
IS  - 0042-9007 (Linking)
VI  - 100
IP  - 1
DP  - 2011 Jan
TI  - Plasmodium falciparum malaria and the immunogenetics of ABO, HLA, and CD36 
      (platelet glycoprotein IV).
PG  - 99-111
LID - 10.1111/j.1423-0410.2010.01429.x [doi]
AB  - Plasmodium falciparum malaria has long been a killer of the young, and has 
      selected for polymorphisms affecting not only erythrocytes, but the 
      immunogenetics of three histocompatibility systems: ABO, human leukocyte antigen 
      (HLA), and CD36. The ABO system is important because the original allele, 
      encoding glycosylation with the A sugar, acts as an adhesion ligand with infected 
      red blood cells (iRBC), thereby promoting vasoocclusion. The prevalence of blood 
      group O, which reduces this cytoadhesion, has increased in endemic areas. Other 
      adaptations which could mitigate A-mediated rosetting include weaker A expression 
      and increased soluble A secretion. The role of the HLA system in malaria has been 
      harder to verify. Although HLA-B53 and DRB1*04 may be associated with clinical 
      outcome, HLA studies are challenged by numerous comparisons in this most 
      polymorphic of systems, and confounded by increasingly heterogeneous populations. 
      Certain HLA markers may also reflect linkage artefact with other malaria-relevant 
      polymorphisms. HLA may be less important because the parasite predominantly 
      invades a compartment which does not express HLA. Adhesion of iRBCs is also 
      mediated by CD36, expressed on platelets, monocytes, and microvascular 
      endothelium. CD36 on monocytes is involved in clearing iRBC, while CD36 on 
      platelets and the endothelium may play a role in tissue sequestration. The 
      genetics of CD36 expression are complex, and recent research is fraught with 
      inconsistent results. The solution may lie in examining genotype-phenotype 
      correlations, zygosity effects on differential tissue expression, or other 
      mechanisms altering CD36 tissue expression. Carefully designed prospective 
      studies should bridge the gap between in-vitro observations and clinical 
      outcomes.
CI  - (c) 2010 The Author(s). Vox Sanguinis (c) 2010 International Society of Blood 
      Transfusion.
FAU - Cserti-Gazdewich, C M
AU  - Cserti-Gazdewich CM
AD  - Department of Medicine (Hematology), University Health Network/Toronto General 
      Hospital, Toronto, ON, Canada.Christine.Cserti@uhn.on.ca
FAU - Mayr, W R
AU  - Mayr WR
FAU - Dzik, W H
AU  - Dzik WH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - England
TA  - Vox Sang
JT  - Vox sanguinis
JID - 0413606
RN  - 0 (ABO Blood-Group System)
RN  - 0 (CD36 Antigens)
RN  - 0 (HLA Antigens)
SB  - IM
MH  - ABO Blood-Group System/genetics
MH  - Animals
MH  - Biological Evolution
MH  - CD36 Antigens/genetics
MH  - Genetic Predisposition to Disease
MH  - HLA Antigens/genetics
MH  - Host-Parasite Interactions/genetics/immunology
MH  - Humans
MH  - Immunogenetic Phenomena
MH  - Malaria, Falciparum/*genetics/*immunology
MH  - Models, Genetic
MH  - Mutation
MH  - Plasmodium falciparum/immunology/pathogenicity
EDAT- 2010/12/24 06:00
MHDA- 2011/04/13 06:00
CRDT- 2010/12/24 06:00
PHST- 2010/12/24 06:00 [entrez]
PHST- 2010/12/24 06:00 [pubmed]
PHST- 2011/04/13 06:00 [medline]
AID - 10.1111/j.1423-0410.2010.01429.x [doi]
PST - ppublish
SO  - Vox Sang. 2011 Jan;100(1):99-111. doi: 10.1111/j.1423-0410.2010.01429.x.