Journal
FRONTIERS IN IMMUNOLOGY
Volume 12, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2021.733136
Keywords
innate lymphoid cell 2; cancer; melanoma; PD-1; TNF-alpha
Categories
Funding
- National Institutes of Health Public Health Service [R01 ES025786, R01 ES021801, R01 HL144790, R01 HL151493, R01 AI145813, R01 HL151769]
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Inhibition of PD-1 on ILC2s suppresses B16 tumor growth and upregulates the production of TNF-alpha, inducing cell death in B16 cells independent of adaptive immunity. These results emphasize the important anti-tumor role of ILC2s in pulmonary B16 cancer progression during PD-1 inhibitory immunotherapy.
While pulmonary ILC2s represent one of the major tissue-resident innate lymphoid cell populations at steady state and are key drivers of cytokine secretion in their occupational niche, their role in pulmonary cancer progression remains unclear. As the programmed cell death protein-1 (PD-1) plays a major role in cancer immunotherapy and immunoregulatory properties, here we investigate the specific effect of PD-1 inhibition on ILC2s during pulmonary B16 melanoma cancer metastasis. We demonstrate that PD-1 inhibition on ILC2s suppresses B16 tumor growth. Further, PD-1 inhibition upregulates pulmonary ILC2-derived TNF-alpha production, a cytotoxic cytokine that directly induces cell death in B16 cells, independent of adaptive immunity. Together, these results highlight the importance of ILC2s and their anti-tumor role in pulmonary B16 cancer progression during PD-1 inhibitory immunotherapy.
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