Figure 4
RBC-specific expression of a model fusion antigen by the HOD mouse. (A) Predicted structure of the HOD antigen. (B) Structure of the HOD construct and amino acid sequence of the HOD antigen. The HOD antigen is under control of the RBC-specific μ′LCR promoter and is a fusion of the full sequence of HEL, a fragment of OVA containing both the OT-I T cell–specific epitope (SIINFEKL) and the OT-II–specific epitope (ISQAVHAAHAEINEAGR), and the human Duffy blood group antigen. Additional features are indicated, including the “Duffy b” polymorphism (D), the first transmembrane domain of the molecule (FFILTSVLGILASSTVLFMLF), and the epitope for the Duffy 3 specific MIMA 29 monoclonal antibody (ALDLLL). The features described in this figure legend are underlined in panel B; amino acids were added at each fusion junction because of introduction of restriction sites Sma I and XhoI (PG and LE, in black). Staining of HOD blood demonstrates the predicted epitopes on RBCs, with no detectable HOD on CD45+TER-119− leukocytes or CD41+TER-119− platelets (C-E). Whereas only the OVA antigen was used in the course of the presented research, the HEL and Duffy antigens were included for alternate research purposes outside the scope of the current report.

RBC-specific expression of a model fusion antigen by the HOD mouse. (A) Predicted structure of the HOD antigen. (B) Structure of the HOD construct and amino acid sequence of the HOD antigen. The HOD antigen is under control of the RBC-specific μ′LCR promoter and is a fusion of the full sequence of HEL, a fragment of OVA containing both the OT-I T cell–specific epitope (SIINFEKL) and the OT-II–specific epitope (ISQAVHAAHAEINEAGR), and the human Duffy blood group antigen. Additional features are indicated, including the “Duffy b” polymorphism (D), the first transmembrane domain of the molecule (FFILTSVLGILASSTVLFMLF), and the epitope for the Duffy 3 specific MIMA 29 monoclonal antibody (ALDLLL). The features described in this figure legend are underlined in panel B; amino acids were added at each fusion junction because of introduction of restriction sites Sma I and XhoI (PG and LE, in black). Staining of HOD blood demonstrates the predicted epitopes on RBCs, with no detectable HOD on CD45+TER-119 leukocytes or CD41+TER-119 platelets (C-E). Whereas only the OVA antigen was used in the course of the presented research, the HEL and Duffy antigens were included for alternate research purposes outside the scope of the current report.

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