The I-Ab-restricted alloresponse of D10.G4.1 T cells is based on the recognition of an endogenous peptide.
TL;DRAbstract
The alloreactivity of T cells is thought to be based on the cross-reactive recognition of allogeneic major histocompatibility complex (MHC) molecules which have bound peptides derived from self antigens or, in the case of cultured T cells, from serum components. While studying the processing requirements of conalbumin (CA) that is recognized by D10.G4.1 T cells in combination with I-Ak molecules we also analysed the cross-reactive stimulation of clone D10.G4.1 T cells by allogeneic, I-Ab expressing stimulator cells which is shown here to be CD4 dependent. In order to distinguish between an endogenous or exogenous origin of a peptide that is presumably co-recognized with I-Ab different types of stimulatory/antigen-presenting cells (APC) were treated with drugs that are known to influence the processing and/or presentation of antigens. It was found that the alloreactive response of D10.G4.1 cells was abolished if the APC were treated with brefeldin A or inhibitors of protein biosynthesis
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The alloreactivity of T cells is thought to be based on the cross-reactive recognition of allogeneic major histocompatibility complex (MHC) molecules which have bound peptides derived from self antigens or, in the case of cultured T cells, from serum components. While studying the processing requirements of conalbumin (CA) that is recognized by D10.G4.1 T cells in combination with I-Ak molecules we also analysed the cross-reactive stimulation of clone D10.G4.1 T cells by allogeneic, I-Ab expressing stimulator cells which is shown here to be CD4 dependent. In order to distinguish between an endogenous or exogenous origin of a peptide that is presumably co-recognized with I-Ab different types of stimulatory/antigen-presenting cells (APC) were treated with drugs that are known to influence the processing and/or presentation of antigens. It was found that the alloreactive response of D10.G4.1 cells was abolished if the APC were treated with brefeldin A or inhibitors of protein biosynthesis
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