JOAO PAULO PORTELA CATANI

(Fonte: Lattes)
Índice h a partir de 2011
6
Lattes
Projetos de Pesquisa
Unidades Organizacionais
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

Filtros

Limpar filtros

Configurações

Colaboração internacional: Austrália ×

Resultados de Busca

Agora exibindo 1 - 2 de 2
  • article 105 Citação(ões) na Scopus
    CCL2/CCR2-Dependent Recruitment of Functional AntigenPresenting Cells into Tumors upon Chemotherapy
    (2014) MA, Yuting; MATTAROLLO, Stephen R.; ADJEMIAN, Sandy; YANG, Heng; AYMERIC, Laetitia; HANNANI, Dalil; CATANI, Joao Paulo Portela; DURET, Helene; TENG, Michele W. L.; KEPP, Oliver; WANG, Yidan; SISTIGU, Antonella; SCHULTZE, Joachim L.; STOLL, Gautier; GALLUZZI, Lorenzo; ZITVOGEL, Laurence; SMYTH, Mark J.; KROEMER, Guido
    The therapeutic efficacy of anthracyclines relies, at least partially, on the induction of a dendritic cell-and T-lymphocyte-dependent anticancer immune response. Here, we show that anthracycline-based chemotherapy promotes the recruitment of functional CD11b(+)CD11c(+)Ly6C(high)Ly6G(-)MHCII(+) dendritic cell-like antigenpresenting cells (APC) into the tumor bed, but not into lymphoid organs. Accordingly, draining lymph nodes turned out to be dispensable for the proliferation of tumor antigen-specific T cells within neoplastic lesions as induced by anthracyclines. In addition, we found that tumors treated with anthracyclines manifest increased expression levels of the chemokine Ccl2. Such a response is important as neoplasms growing in Ccl2(-/-) mice failed to accumulate dendritic cell-like APCs in response to chemotherapy. Moreover, cancers developing in mice lacking Ccl2 or its receptor (Ccr2) exhibited suboptimal therapeutic responses to anthracycline-based chemotherapy. Altogether, our results underscore the importance of the CCL2/CCR2 signaling axis for therapeutic anticancer immune responses as elicited by immunogenic chemotherapy. (C) 2013 AACR.
  • 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.