JOAO PAULO PORTELA CATANI

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Instituto do Câncer do Estado de São Paulo, Hospital das Clínicas, Faculdade de Medicina
LIM/24 - Laboratório de Oncologia Experimental, Hospital das Clínicas, Faculdade de Medicina

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  • article 537 Citação(ões) na Scopus
    Anticancer Chemotherapy-Induced Intratumoral Recruitment and Differentiation of Antigen-Presenting Cells
    (2013) MA, Yuting; ADJEMIAN, Sandy; MATTAROLLO, Stephen R.; YAMAZAKI, Takahiro; AYMERIC, Laetitia; YANG, Heng; CATANI, Joao Paulo Portela; HANNANI, Dalil; DURET, Helene; STEEGH, Kim; MARTINS, Isabelle; SCHLEMMER, Frederic; MICHAUD, Mickael; KEPP, Oliver; SUKKURWALA, Abdul Qader; MENGER, Laurie; VACCHELLI, Erika; DROIN, Nathalie; GALLUZZI, Lorenzo; KRZYSIEK, Roman; GORDON, Siamon; TAYLOR, Philip R.; ENDERT, Peter Van; SOLARY, Eric; SMYTH, Mark J.; ZITVOGEL, Laurence; KROEMER, Guido
    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.