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.
© 2010 The Author(s). Vox Sanguinis © 2010 International Society of Blood Transfusion.