Title of article :
Natural killer cell receptor—Repertoire and functions after induction therapy by polyclonal rabbit anti-thymocyte globulin in unsensitized kidney transplant recipients
Author/Authors :
Pierre Hadaya، نويسنده , , Karine and Avila، نويسنده , , Yannick and Valloton، نويسنده , , Laure and de Rham، نويسنده , , Casimir and Bandelier، نويسنده , , Cedric and Ferrari-Lacraz، نويسنده , , Sylvie and Pascual، نويسنده , , Manuel and Pantaleo، نويسنده , , Giuseppe and Martin، نويسنده , , Pierre-Yves and Buhler، نويسنده , , Leo and Villard، نويسنده , , Jean، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2010
Pages :
11
From page :
250
To page :
260
Abstract :
Polyclonal rabbit anti-thymocyte globulin (rATG) is widely used in solid organ transplantation (SOT) as induction therapy or to treat corticosteroid-resistant rejection. In vivo, the effect of rATG on natural killer (NK) cells has not been studied. These cells are of particular relevance after SOT because classical immunosuppressive drugs do not inhibit or even can activate NK cells. A cohort of 20 recipients at low immunological risk, that had been receiving rATG as induction therapy, was analyzed for receptor repertoire, cytotoxicity and capacity of NK cells to secrete IFN-γ before kidney transplantation and at different time points thereafter. NK cells expressed fewer killer-cell immunoglobulin-like receptors (KIR), fewer activating receptors NKG2D, but more inhibitory receptor NKG2A compatible with an immature phenotype in the first 6 months post transplantation. Both cytotoxicity of NK cells and the secretion of IFN-γ were preserved over time after transplantation.
Keywords :
Infection , Alloimmune response , Killer-cell immunoglobulin-like receptors (KIR) , Natural cytotoxic receptors , Kidney Transplantation , natural killer cells , C-type lectin receptor , immunosuppression , Polyclonal rabbit anti-thymocyte globulin (rATG )
Journal title :
Clinical Immunology
Serial Year :
2010
Journal title :
Clinical Immunology
Record number :
1854781
Link To Document :
بازگشت