Journal
IMMUNITY
Volume 43, Issue 3, Pages 579-590Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2015.08.006
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Funding
- NCI Cancer Center Support Grant [P30-CA14051]
- Howard Hughes Medical Institute
- NIH [1 U54 CA126515-01, R01-CA185020-01, T32 GM007753]
- Damon Runyon Cancer Foundation
- Margaret A. Cunningham Immune Mechanisms in Cancer Research Fellowship Award
- Lung Cancer Research Foundation
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Infiltration of regulatory T (Treg) cells into many tumor types correlates with poor patient prognoses. However, mechanisms of intratumoral Treg cell function remain to be elucidated. We investigated Treg cell function in a genetically engineered mouse model of lung adenocarcinoma and found that Treg cells suppressed anti-tumor responses in tumor-associated tertiary lymphoid structures (TA-TLSs). TA-TLSs have been described in human lung cancers, but their function remains to be determined. TLSs in this model were spatially associated with > 90% of tumors and facilitated interactions between T cells and tumor-antigen-presenting dendritic cells (DCs). Costimulatory ligand expression by DCs and T cell proliferation rates increased in TA-TLSs upon Treg cell depletion, leading to tumor destruction. Thus, we propose that Treg cells in TA-TLSs can inhibit endogenous immune responses against tumors, and targeting these cells might provide therapeutic benefit for cancer patients.
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