期刊
IMMUNITY
卷 38, 期 4, 页码 729-741出版社
CELL PRESS
DOI: 10.1016/j.immuni.2013.03.003
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资金
- European Commission (ArtForce)
- Agence National de la Recherche (ANR)
- Ligue contre le Cancer (Equipe labellisee)
- Fondation pour la Recherche Medicale (FRM)
- Institut National du Cancer (INCa)
- Association pour la Recherche sur le Cancer (ARC) LabEx Immuno-Oncologie
- Fondation de France
- Fondation Bettencourt-Schueller
- AXA Chair for Longevity Research
- Canceropole Ile-de-France
- Paris Alliance of Cancer Research Institutes (PACRI)
- China Scholarship Council (CSC)
- Ligue Nationale contre le Cancer
- Coordenacao de Aperfeicoamento Pessoal de Nivel Superior (CAPES/Brazil)
- ARC
- National Health and Medical Research Council (NHMRC)
- Victorian Cancer Agency
- MRC [G0601617] Funding Source: UKRI
- Medical Research Council [G0601617] Funding Source: researchfish
The therapeutic efficacy of anthracyclines relies on antitumor immune responses elicited by dying cancer cells. How chemotherapy-induced cell death leads to efficient antigen presentation to T cells, however, remains a conundrum. We found that intra-tumoral CD11c(+)CD11b(+)Ly6C(hi) cells, which displayed some characteristics of inflammatory dendritic cells and included granulomonocytic precursors, were crucial for anthracycline-induced anticancer immune responses. ATP released by dying cancer cells recruited myeloid cells into tumors and stimulated the local differentiation of CD11c(+)CD11b(+)Ly6C(hi) cells. Such cells efficiently engulfed tumor antigens in situ and presented them to T lymphocytes, thus vaccinating mice, upon adoptive transfer, against a challenge with cancer cells. Manipulations preventing tumor infiltration by CD11c(+)CD11b(+)Ly6C(hi) cells, such as the local overexpression of ectonucleotidases, the blockade of purinergic receptors, or the neutralization of CD11b, abolished the immune system-dependent antitumor activity of anthracyclines. Our results identify a subset of tumor-infiltrating leukocytes as therapy-relevant antigen-presenting cells.
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