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Vox Sang ; 99(4): 369-74, 2010 Nov.
Article in English | MEDLINE | ID: mdl-20546207

ABSTRACT

BACKGROUND AND OBJECTIVES: Transfusion of allogeneic platelet products can result in antibodies against donor major histocompatibility complex (MHC) I antigens, leading to a refractory state to subsequent platelet transfusions. However, there is disagreement in the field regarding the molecular mechanisms of humoral alloimmunization. One hypothesis states that donor MHC II is a requirement for alloimmunization. However, other studies have suggested that donor MHC I is alone sufficient and MHC II is not required. MATERIALS AND METHODS: We utilized a mouse model of anti-MHC I alloimmunization to transfused blood, which employed donors with a complete deletion of all MHC II genes. BALB/c (H-2(d)) recipients were transfused with blood from either C57BL/6 (H-2(b)) or MHC II null donors on a C57BL/6 background. Anti-MHC I alloimmunization was monitored by indirect immunofluorescence. RESULTS: Recipients of either wild type or MHC II null blood produced equivalent humoral responses against donor MHC I antigens. However, there was variation in the relative amounts of IgG subclasses. CONCLUSION: These data reject the hypothesis that donor MHC II expression is required for alloimmunization to MHC I antigens.


Subject(s)
Histocompatibility Antigens Class II/immunology , Histocompatibility Antigens Class I/immunology , Platelet Transfusion , ABO Blood-Group System , Animals , Galactosyltransferases/immunology , Mice , Mice, Inbred BALB C
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