Defunctioning polymorphism in the immunoglobulin G inhibitory receptor (FcγRIIB-T/T232) does not impact on kidney transplant or recipient survival
Background - There is an increasing appreciation of the deleterious effects of antibody and B cells on acute and chronic transplant outcomes. Many effector functions of antibody are mediated by a family of receptors (FcγRs) that are expressed on most immune cells, including neutrophils, nat...
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| Hauptverfasser: | , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
2014
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| In: |
Transplantation
Year: 2014, Jahrgang: 98, Heft: 3, Pages: 285-291 |
| ISSN: | 1534-6080 |
| DOI: | 10.1097/TP.0000000000000287 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1097/TP.0000000000000287 Verlag, lizenzpflichtig, Volltext: https://journals.lww.com/transplantjournal/Fulltext/2014/08150/Defunctioning_Polymorphism_in_the_Immunoglobulin_G.11.aspx 
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| Verfasserangaben: | Menna R. Clatworthy, Rebeccah J. Matthews, Bernd Doehler, Lisa C. Willcocks, Gerhard Opelz, and Kenneth G.C. Smith |
MARC
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| 245 | 1 | 0 | |a Defunctioning polymorphism in the immunoglobulin G inhibitory receptor (FcγRIIB-T/T232) does not impact on kidney transplant or recipient survival |c Menna R. Clatworthy, Rebeccah J. Matthews, Bernd Doehler, Lisa C. Willcocks, Gerhard Opelz, and Kenneth G.C. Smith |
| 246 | 3 | 3 | |a Defunctioning polymorphism in the immunoglobulin G inhibitory receptor (Fc gamma RIIB-T/T two hundred thirty-two) does not impact on kidney transplant or recipient survival |
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| 520 | |a Background - There is an increasing appreciation of the deleterious effects of antibody and B cells on acute and chronic transplant outcomes. Many effector functions of antibody are mediated by a family of receptors (FcγRs) that are expressed on most immune cells, including neutrophils, natural killer cells, and B cells. Most FcγRs are activating and controlled by a single inhibitory receptor, FcγRIIB (CD32B), which also regulates some aspects of B-cell activation and antibody production. FcγRIIB-deficient mice develop severe chronic arteriopathy in a murine cardiac allograft model. A single nucleotide polymorphism in human FcγRIIB (rs1050501) results in profound receptor dysfunction and is associated with systemic lupus erythematosus. The frequency of this FcγRIIB-I/T232 polymorphism also shows significant racial variation. - Methods - In the present study, we sought to determine whether the FcγRIIB-I/T232 single nucleotide polymorphism rs1050501 affected susceptibility to renal allograft rejection or loss and transplant recipient survival. FcγRIIB-I/T232 genotype was determined in 2,851 Caucasian and 570 Afro-Caribbean renal transplant recipients, and in 236 transplant recipients with a primary diagnosis of systemic lupus erythematosus, all of whom were enrolled into the Collaborative Transplant Study. - Results - We found no significant difference in pretransplant panel reactive antibodies, acute rejection at 1-year nor in 10-year transplant or patient survival in individuals with differing FcγRIIB-I/T232 genotype. - Conclusion - This negative result is surprising, given the importance of this receptor in modulating antibody effector function. | ||
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| 700 | 1 | |a Doehler, Bernd |e VerfasserIn |4 aut | |
| 700 | 1 | |a Willcocks, Lisa C. |e VerfasserIn |4 aut | |
| 700 | 1 | |a Opelz, Gerhard |d 1944- |e VerfasserIn |0 (DE-588)1026480345 |0 (DE-627)726772453 |0 (DE-576)371826527 |4 aut | |
| 700 | 1 | |a Smith, Kenneth G. C. |e VerfasserIn |4 aut | |
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