C R Gilson1, C M Cadwell, N H Smith, J E Hendrickson, J C Zimring. 1. Center for Transfusion and Cellular Therapies, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, Georgia, USA.
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.
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 donorMHC 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 donorMHC II expression is required for alloimmunization to MHC I antigens.
Authors: B Pérarnau; M F Saron; B Reina San Martin; N Bervas; H Ong; M J Soloski; A G Smith; J M Ure; J E Gairin; F A Lemonnier Journal: Eur J Immunol Date: 1999-04 Impact factor: 5.532
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Authors: Krystalyn E Hudson; Andrea S L Wong; Amanda L Richards; Linda M Kapp; James C Zimring Journal: Transfusion Date: 2019-01-25 Impact factor: 3.157