-318C/T polymorphism of the CTLA-4 gene is an independent risk factor for RBC alloimmunization among sickle cell disease patients

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art_OLIVEIRA_318CT_polymorphism_of_the_CTLA4_gene_is_an_2017.PDF (665.22 KB)
Citações na Scopus
16
Tipo de produção
article
Data de publicação
2017
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
WILEY
Autores
OLIVEIRA, V. B.
GOMES, F. C. A.
Citação
INTERNATIONAL JOURNAL OF IMMUNOGENETICS, v.44, n.5, p.219-224, 2017
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) molecule is expressed on T-lymphocyte membrane and negatively influences the antigen-presenting process. Reduced expression of CTLA-4 due to gene polymorphisms is associated with increased risk of autoimmune disorders, whose physiopathology is similar to that of post-transfusion red blood cell (RBC) alloimmunization. Our goal was to evaluate if polymorphisms of CTLA-4 gene that affect protein expression are associated with RBC alloimmunization. This was a case-control study in which 134 sickle cell disease (SCD) patients and 253 non-SCD patients were included. All patients were genotyped for the polymorphisms 49A/G and -318C/T of CTLA-4 gene. The genotype frequency of -318C/T differed significantly between alloimmunized and nonalloimmunized SCD patients, irrespective of clinical confounders (p=.016). SCD patients heterozygous for -318T allele presented higher risk of alloantibody development (OR: 5.4, CI: 1.15-25.6). In conclusion, the polymorphism -318C/T of CTLA-4 gene is associated with RBC alloimmunization among SCD patients. This highlights the role played by CTLA-4 on post-transfusion alloantibody development.
Palavras-chave
alloimmunization, CTLA-4, polymorphism, sickle cell
URI
https://observatorio.fm.usp.br/handle/OPI/21815
Referências
  1. Bour-Jordan H, 2003, NAT IMMUNOL, V4, P182, DOI 10.1038/ni884
  2. Dezan MR, 2017, BLOOD CELL MOL DIS, V65, P8, DOI 10.1016/j.bcmd.2017.03.014
  3. Dezan M. R., 2016, ISBT SCI SERIES, V11, P132
  4. Dinardo Carla Luana, 2013, Rev. Bras. Hematol. Hemoter., V35, P414, DOI 10.5581/1516-8484.20130123
  5. Fasano RM, 2015, BRIT J HAEMATOL, V168, P291, DOI 10.1111/bjh.13123
  6. Gilson CR, 2012, TRANSFUSION, V52, P2209, DOI 10.1111/j.1537-2995.2011.03550.x
  7. Hendrickson JE, 2006, TRANSFUSION, V46, P1526, DOI 10.1111/j.1537-2995.2006.00946.x
  8. Hendrickson JE, 2012, TRANSFUSION, V52, P231, DOI 10.1111/j.1537-2995.2011.03255.x
  9. Higgins JM, 2008, BLOOD, V112, P2546, DOI 10.1182/blood-2008-03-146415
  10. Kumar N, 2015, INT J IMMUNOGENET, V42, P445, DOI 10.1111/iji.12233
  11. Nickel RS, 2016, TRANSFUSION, V56, P107, DOI 10.1111/trf.13379
  12. Noizat-Pirenne F, 2006, TRANSFUSION, V46, P1328, DOI 10.1111/j.1537-2995.2006.00900.x
  13. Park YJ, 2000, THYROID, V10, P453
  14. Rodriguez S, 2009, AM J EPIDEMIOL, V169, P505, DOI 10.1093/aje/kwn359
  15. ROSSE WF, 1990, BLOOD, V76, P1431
  16. Ryder AB, 2016, BRIT J HAEMATOL, V174, P483, DOI 10.1111/bjh.13781
  17. Sippert EA, 2016, TRANSFUSION, V56, p32A
  18. Svahn J, 2005, BONE MARROW TRANSPL, V35, pS89, DOI 10.1038/sj.bmt.1704855
  19. Ting WH, 2016, PLOS ONE, V11, DOI 10.1371/journal.pone.0154394
  20. Ueda H, 2003, NATURE, V423, P506, DOI 10.1038/nature01621
  21. Verduin EP, 2016, TRANSFUSION, V56, P1849, DOI 10.1111/trf.13648
  22. Vichinsky E P, 2012, Immunohematology, V28, P20
  23. Vingert B, 2014, AM J HEMATOL, V89, P261, DOI 10.1002/ajh.23629
  24. Yu J, 2007, AM J HEMATOL, V82, P691, DOI 10.1002/ajh.20959

Coleções
Artigos e Materiais de Revistas Científicas - FM/MCM
Artigos e Materiais de Revistas Científicas - FM/MCP
Artigos e Materiais de Revistas Científicas - FM/MIP
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - LIM/13
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