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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Human monocytes but not dendritic cells are killed by blocking of autocrine cyclooxygenase activity

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Autor(es):
Oliveira, Bruno L. ; Cavalcanti, Clara M. ; Azevedo, Ana Paula S. ; Tomiyoshi, Marcio Y. ; Bergami-Santos, Patricia C. ; Barbuto, Jose Alexandre M. [1]
Número total de Autores: 6
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Dept Immunol, Inst Ciencias Biomed, Lab Tumor Immunol, BR-05508000 Sao Paulo - Brazil
Número total de Afiliações: 1
Tipo de documento: Artigo Científico
Fonte: Cellular Immunology; v. 258, n. 1, p. 107-114, 2009.
Citações Web of Science: 2
Resumo

Dendritic cells (DCs), in peripheral tissues, derive mostly from blood precursors that differentiate into DCs under the influence of the local microenvironment. Monocytes constitute the main known DC precursors in blood and their infiltration into tissues is up-regulated during inflammation. During this process, the local production of mediators, like prostaglandins (PGs), influence significantly DC differentiation and function. In the present paper we show that treatment of blood adherent mononuclear cells with 10 mu M indomethacin, a dose achieved in human therapeutic settings, causes monocytes' progressive death but does not affect DCs viability or cell surface phenotype. This resistance of DCs was observed both for cells differentiated in vitro from blood monocytes and for a population with DCs characteristics already present in blood. This phenomenon could affect the local balance of antigen-presenting cells, influence the induction and pattern of immune responses developed under the treatment with non-steroidal anti-inflammatory drugs and, therefore, deserves further investigation. (C) 2009 Elsevier Inc. All rights reserved. (AU)

Processo FAPESP: 04/09956-0 - Modulação funcional de células dentríticas em diferentes situações fisiopatológicas
Beneficiário:Jose Alexandre Marzagão Barbuto
Modalidade de apoio: Auxílio à Pesquisa - Temático