Abstract
Meeting abstracts Although cytotoxic CD8 T lymphocytes (CTL) were historically considered primary effectors of antitumor immunity, solely boosting CTL responses with CD8 vaccines in various tumor types has yielded unpredictable clinical results, possibly because CTLs function suboptimally without
Highlights
Cytotoxic CD8 T lymphocytes (CTL) were historically considered primary effectors of antitumor immunity, solely boosting CTL responses with CD8 vaccines in various tumor types has yielded unpredictable clinical results, possibly because CTLs function suboptimally without adequate CD4 T lymphocyte help
Th1 sensitization was initially performed in 5 breast cancer patients with known anti-HER3 reactivity in order to identify single immunogenic HER3 CD4 epitopes
HER3 extracellular domain (ECD)-specific CD4 Th1 were sequentially restimulated against 10-peptide clusters, narrowed to 3-peptide clusters, and to single immunogenic HER3 peptides
Summary
Cytotoxic CD8 T lymphocytes (CTL) were historically considered primary effectors of antitumor immunity, solely boosting CTL responses with CD8 vaccines in various tumor types has yielded unpredictable clinical results, possibly because CTLs function suboptimally without adequate CD4 T lymphocyte help. CD4 T-helper type 1 (Th1) cells secrete INF-g/TNF-a, inducing tumor senescence and apoptosis. Successful incorporation of CD4 epitopes into cancer vaccine construction and generation of durable antigen-specific CD4 immunity remains a challenge. Using the extracellular domain (ECD) of HER3 as a candidate “oncodriver” tumor antigen, we sought to identify immunogenic HER3 peptides that demonstrate Class II promiscuity and generate anti-HER3 CD4 immunity for inclusion in vaccine development
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