HLA-F
KIR3DS1
LILRB1
alloimmunisation
genetic polymorphisms
sickle cell disease
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
02 Sep 2023
02 Sep 2023
Historique:
received:
26
07
2023
revised:
25
08
2023
accepted:
31
08
2023
medline:
11
9
2023
pubmed:
9
9
2023
entrez:
9
9
2023
Statut:
epublish
Résumé
Red blood cell (RBC) transfusion remains a critical component in caring for the acute and chronic complications of sickle cell disease (SCD). Patient alloimmunisation is the main limitation of transfusion, which can worsen anaemia and lead to delayed haemolytic transfusion reaction or transfusion deadlock. Although biological risk factors have been identified for immunisation, patient alloimmunisation remains difficult to predict. We aimed to characterise genetic alloimmunisation factors to optimise the management of blood products compatible with extended antigen matching to ensure the self-sufficiency of labile blood products. Considering alloimmunisation in other clinical settings, like pregnancy and transplantation, many studies have shown that HLA Ib molecules (HLA-G, -E, and -F) are involved in tolerance mechanism; these molecules are ligands of immune effector cell receptors (LILRB1, LILRB2, and KIR3DS1). Genetic polymorphisms of these ligands and receptors have been linked to their expression levels and their influence on inflammatory and immune response modulation. Our hypothesis was that polymorphisms of
Identifiants
pubmed: 37686397
pii: ijms241713591
doi: 10.3390/ijms241713591
pmc: PMC10487752
pii:
doi:
Substances chimiques
HLA-F antigens
0
Leukocyte Immunoglobulin-like Receptor B1
0
Ligands
0
LILRB1 protein, human
0
Antigens, CD
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
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