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However, frequent blood transfusion poses the risk of alloimmunization. On average, 30% of SCD patients will alloimmunize while other patient groups form antibodies less frequently. Identification of genetic markers may help to predict which patients are at risk to form alloantibodies. The aim of this study was to evaluate whether genetic variations in the Toll\u2010like receptor pathway or in genes previously associated with antibody\u2010mediated conditions are associated with red blood cell (RBC) alloimmunization in a cohort of SCD patients. In this case\u2010control study, cases had a documented history of alloimmunization while controls had received \u226520 RBC units without alloantibody formation. We used a customized single nucleotide polymorphism (SNP) panel to genotype 690 SNPs in 275 (130 controls, 145 cases) patients. Frequencies were compared using multiple logistic regression analysis. In our primary analysis, no SNPs were found to be significantly associated with alloimmunization after correction for multiple testing. However, in a secondary analysis with a less stringent threshold for significance we found 19 moderately associated SNPs. Among others, SNPs in <jats:italic>TLR1\/TANK<\/jats:italic> and <jats:italic>MALT1<\/jats:italic> were associated with a higher alloimmunization risk, while SNPs in <jats:italic>STAM\/IFNAR1<\/jats:italic> and <jats:italic>STAT4<\/jats:italic> conferred a lower alloimmunization risk.<\/jats:p>","DOI":"10.1111\/bjh.15998","type":"journal-article","created":{"date-parts":[[2019,6,6]],"date-time":"2019-06-06T02:04:47Z","timestamp":1559786687000},"page":"887-899","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Identification of genetic biomarkers for alloimmunization in sickle cell disease"],"prefix":"10.1111","volume":"186","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8881-795X","authenticated-orcid":false,"given":"Sanne M.","family":"Meinderts","sequence":"first","affiliation":[{"name":"Department of Blood Cell Research, Sanquin Research and Landsteiner Laboratory, Academic Medical Centre University of Amsterdam Amsterdam the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jorn J.","family":"Gerritsma","sequence":"additional","affiliation":[{"name":"Department of Paediatric Haematology, Immunology and Infectious Diseases, Emma Children\u2019s Hospital, Academic Medical Centre University of Amsterdam Amsterdam the Netherlands"},{"name":"Department of Plasma Proteins, Sanquin Research and Landsteiner Laboratory, Academic Medical Centre Univsersity of Amsterdam Amsterdam the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joep W. R.","family":"Sins","sequence":"additional","affiliation":[{"name":"Department of Paediatric Haematology, Immunology and Infectious Diseases, Emma Children\u2019s Hospital, Academic Medical Centre University of Amsterdam Amsterdam the Netherlands"},{"name":"Department of Plasma Proteins, Sanquin Research and Landsteiner Laboratory, Academic Medical Centre Univsersity of Amsterdam Amsterdam the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"de Boer","sequence":"additional","affiliation":[{"name":"Department of Blood Cell Research, Sanquin Research and Landsteiner Laboratory, Academic Medical Centre University of Amsterdam Amsterdam the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karin","family":"van Leeuwen","sequence":"additional","affiliation":[{"name":"Department of Blood Cell Research, Sanquin Research and Landsteiner Laboratory, Academic Medical Centre University of Amsterdam Amsterdam the 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