Monocyte-derived dendritic cells in malaria

Autor(es)

Hirako, Isabella C. ^{[1, 2]} ; Assis, Patricia A. ^[2] ; Galvao-Filho, Bruno ^[1] ; Luster, Andrew D. ^{[3, 4]} ; Antonellil, Lis R. V. ^[1] ; Gazzinelli, Ricardo T. ^{[1, 2, 5]}

Afiliação do(s) autor(es)

^[1] Fundacao Oswaldo Cruz Minas, BR-30190002 Belo Horizonte, MG - Brazil

^[2] Univ Massachusetts, Med Sch, Worcester, MA 01605 - USA

^[3] Massachusetts Gen Hosp, Boston, MA 02114 - USA

^[4] Harvard Med Sch, Boston, MA 02115 - USA

^[5] Fundacao Oswaldo Cruz, Plataforma Med Translac, BR-14049900 Ribeirao Preto, SP - Brazil

• Tipo de documento: Artigo de Revisão
• Fonte: Current Opinion in Microbiology; v. 52, p. 139-150, DEC 2019.
• Citações Web of Science: 0

Resumo

The pathogenesis of malaria is a multifactorial syndrome associated with a deleterious inflammatory response that is responsible for many of the clinical manifestations. While dendritic cells (DCs) play a critical role in initiating acquired immunity and host resistance to infection, they also play a pathogenic role in inflammatory diseases. In our recent studies, we found in different rodent malaria models that the monocyte-derived DCs (MO-DCs) become, transiently, a main DC population in spleens and inflamed non-lymphoid organs. These studies suggest that acute infection with Plasmodium berghei promotes the differentiation of splenic monocytes into inflammatory monocytes (iMOs) and thereafter into MO-DCs that play a pathogenic role by promoting inflammation and tissue damage. The recruitment of MO-DCs to the lungs and brain are dependent on expression of CCR4 and CCR5, respectively, and expression of respective chemokine ligands in each organ. Once they reach the target organ the MO-DCs produce the CXCR3 ligands (CXCL9 and CXCL10), recruit CD8 T cells, and produce toxic metabolites that play an important role in the development of experimental cerebral malaria (ECM) and acute respiratory distress syndrome (ARDS). (AU)

• Processo FAPESP: 16/23618-8 - Mecanismos imunológicos de resistência e patogênese da malária
• Beneficiário: João Santana da Silva
• Modalidade de apoio: Auxílio à Pesquisa - Temático