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- W4313386328 abstract "Abstract Patients with BCR-ABL+ acute lymphoblastic leukemia develop T cell responses to the BCR-ABL fusion peptide (referred to as BAp). However, these responses are not sustained and loss of the BAp-specific T cell response correlates with relapse. A major gap in our knowledge is why such epitopes do not elicit immune responses that eliminate BCR-ABL+ leukemia. This knowledge gap exists because of an inability to track the fates of endogenous BAp:I-Ab-specific T cells in vivo. To address this question we plan to generate peptide:MHCII tetramers that will allow us to track BAp:I-Ab-specific T cell responses. We have demonstrated that CD4+ T cells exist that recognize the BCR-ABL fusion junction in a mouse model of BCR-ABL+ leukemia. We are generating BAp:I-Ab tetramers that will allow us to track these cells in vivo. Using this reagent we will determine whether T cell responses are impaired due to deletion, immune deviation, Treg-mediated suppression or anergy. We will then assess whether enhancing antigen presentation or inhibiting anergy improves BAp:I-Ab-specific T cell responses. In addition, we will determine if altering the cytokine mileu can improve the CD4+ T cell response to BCR-ABL+ leukemia using both knock-out mouse mice and in vivo delivery of exogenous cytokines." @default.
- W4313386328 created "2023-01-06" @default.
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- W4313386328 date "2013-05-01" @default.
- W4313386328 modified "2023-09-27" @default.
- W4313386328 title "Tracking the CD4+ T cell response to BCR-ABL-induced leukemia (P4330)" @default.
- W4313386328 doi "https://doi.org/10.4049/jimmunol.190.supp.45.13" @default.
- W4313386328 hasPublicationYear "2013" @default.
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