Journal
JOURNAL OF IMMUNOLOGY
Volume 164, Issue 2, Pages 562-565Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.164.2.562
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Funding
- Intramural NIH HHS [Z01 BC010763-01, Z99 CA999999] Funding Source: Medline
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Neoantigens resulting from the inherent genomic instability of tumor cells generally do not trigger immune recognition. Similarly, transfection of tumors with model Ags often fails to elicit CD8(+) T cell responses or alter a tumor's growth rate or lethality. We report here that the adoptive transfer of activated Th1-type CD4(+) T cells specific for a model tumor Ag results in the de novo generation of CD8(+) T cells with specificity to that Ag and concomitant tumor destruction. The anti-tumor effects of the CD4(+) T cells required the presence of both MHC class I and class II on host cells, as evidenced by experiments in knockout mice, suggesting that CD4(+) T cells enhanced the ability of host APC to activate endogenous CD8(+) T cells. These results indicate that the apparent inability of tumor cells expressing highly immunogenic epitopes to activate tumor-specific CD8(+) T cells can be altered by activated CD4(+) T cells.
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