FREQUENCY OF FCGRIIIA POLYMORPHISMS IN NONT CELL DEPLETED HAPLOIDENTICAL STEM CELL TRANSPLANTATION (Abstract in rivista)

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Label
  • FREQUENCY OF FCGRIIIA POLYMORPHISMS IN NONT CELL DEPLETED HAPLOIDENTICAL STEM CELL TRANSPLANTATION (Abstract in rivista) (literal)
Anno
  • 2012-01-01T00:00:00+01:00 (literal)
Alternative label
  • Anna Aureli1, Angelica Canossi1, Tiziana Del Beato1,Roberto Arriga2, Stella Santarone3, Paolo Di Bartolomeo3, Franco Papola4, William Arcese5, Giuseppe Sconocchia6 (2012)
    FREQUENCY OF FCGRIIIA POLYMORPHISMS IN NONT CELL DEPLETED HAPLOIDENTICAL STEM CELL TRANSPLANTATION
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Anna Aureli1, Angelica Canossi1, Tiziana Del Beato1,Roberto Arriga2, Stella Santarone3, Paolo Di Bartolomeo3, Franco Papola4, William Arcese5, Giuseppe Sconocchia6 (literal)
Pagina inizio
  • 465 (literal)
Pagina fine
  • 466 (literal)
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  • 79 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
  • 6 (literal)
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  • 1CNR Institute of Translational Pharmacology, L'Aquila, Italy, 2Tor Vergata University, Rome, Italy, 3Center of Bone Marrow Transplant, Pescara, Italy, 4CRITT S. Salvatore Hospital, L'Aquila, Italy, 5Rome Transplant Network, Rome, Italy, 6CNR Institute of Translational Pharmacology, Rome, Italy (literal)
Titolo
  • FREQUENCY OF FCGRIIIA POLYMORPHISMS IN NONT CELL DEPLETED HAPLOIDENTICAL STEM CELL TRANSPLANTATION (literal)
Abstract
  • Due to the lack of HLA-matched donors, haploidentical related donor transplantation (HSCT) has been increasingly utilized in high-risk hematologic patients. Recent evidences suggest that non-HLA immune-associated genes are also implicated in the clinical outcome after allo-SCT. In our laboratory, we are interested in studying the FcgammaRIII A (CD16), a low affinity receptor for monomeric IgG, preferentially expressed on NK cells, and on subsets of monocytes and T cells. According to the literature, CD16 is mainly composed of 5 polymorphic molecules with a variable binding affinity for the IgG Fc fragment which could lead to a modulation of antibody dependenT cellular cytotoxicity (ADCC). Since there is evidence that CD16A-158V/F and CD16A-48L/H/R polymorphisms could influencethe outcome of homozygous leukemic patients undergoing HLAfully matched unrelated SCT transplantation, we have hypothesizedthat CD16A polymorphisms could also have an impact onnon T cell depleted HSCT outcome. In this preliminary study,we have evaluated the frequency of CD16 polymorphisms in16 unmanipulated donor/recipient pairs. DNA was isolated fromperipheral blood, and CD16A-48 and -158 polymorphisms wereanalyzed utilizing a sequence based typing (SBT) assay. Whenpossible, the indicated CD16 polymorphisms were evaluatedbefore, and 1, 3 and 12 months after transplant. Eight patientsare alive and disease-free with a median follow-up of 12 months,4 died of acute GvHD and 4 died of infections. Seventy fivepercent of recipients (12) and 69% of donors (11) had CD16AA-158V/F respectively, while 25% of recipients (4) and 31% ofdonors (5) had CD16A-158V/V respectively. Interestingly, noneof recipients and donors had CD16A-158F/F. In recipients,CD16A-48 polymorphism included 68% L/L (11), 6% L/H (1),19% L/R (3) and 6% H/R (1) while donors CD16A48 involved75% L/L (12), 6% L/H (1), 12.5% LR (2), and 0%H/R. A clearlinkage between the CD16A-48 and CD16A-158 polymorphismswas observed since 10 of 16 patients with CD16A-158F/V werealso CD16A-48L/L. In addition, since there were only 3 informativedonor/recipient pairs with differences in CD16A polymorphisms,of which only 1 patient survived, it would be criticalto increase case numbers in order to understand the influence of donor mis-matched CD16A genotype on clinical transplantation outcomes. (literal)
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