Journal
CURRENT OPINION IN IMMUNOLOGY
Volume 47, Issue -, Pages 85-92Publisher
CURRENT BIOLOGY LTD
DOI: 10.1016/j.coi.2017.07.004
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Funding
- National Institutes of Health [R01 CA178846, P30 CA044579]
- Cancer Research Institute Clinical Laboratory Integration Project (CLIP)
- NATIONAL CANCER INSTITUTE [R01CA178846, P30CA044579] Funding Source: NIH RePORTER
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There are compelling arguments for designing cancer vaccines specifically to induce CD4(+) helper T cell responses. Recent studies highlight the crucial role of proliferating, activated effector memory TM CD4(+) T cells in effective antitumor immunity and reveal that CD4(+) T cells induce more durable immune-mediated tumor control than CD8(+) T cells. CD4(+) T cells promote antitumor immunity by numerous mechanisms including enhancing antigen presentation, co-stimulation, T cell homing, T cell activation, and effector function. These effects are mediated at sites of T cell priming and at the tumor microenvironment. Several cancer vaccine approaches induce durable CD4(+) T cell responses and have promising clinical activity. Future work should further optimize vaccine adjuvants and combination therapies incorporating helper peptide vaccines.
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