Control of infection by pyroptosis and autophagy: role of TLR and NLR

Control of infection by pyroptosis and autophagy: role of TLR and NLR

Autor Bortoluci, Karina R. Autor UNIFESP Google Scholar
Medzhitov, Ruslan Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Howard Hughes Med Inst
Yale Univ
Resumo Cells can die by distinct mechanisms with particular impacts on the immune response. in addition to apoptosis and necrosis, recent studies lead to characterization of a new pro-inflammatory form of cell death, pyroptosis. TLR and NLR, central innate immune sensors, can control infections by modulating host cell survival. in addition, TLRs can promote the induction of autophagy, thus promoting delivery of infecting pathogens to the lysosomes. On the other hand, activation of some NLR members, especially NLRC4 and NAIP5, leads to the infected cell death by pyroptosis, which is accompanied by secretion of the pro-inflammatory cytokines IL-1 beta, IL-18, and IL-33. Data presented here illustrate how the compartmentalization of the innate immune sensors can influence the outcome of infections by controlling the fate of host cells.
Palavra-chave TLR
NLR
Pyroptosis
Autophagy
Cell death
Inflammasomes
Idioma Inglês
Financiador Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Data de publicação 2010-05-01
Publicado em Cellular and Molecular Life Sciences. Basel: Springer Basel Ag, v. 67, n. 10, p. 1643-1651, 2010.
ISSN 1420-682X (Sherpa/Romeo, fator de impacto)
Publicador Springer
Extensão 1643-1651
Fonte http://dx.doi.org/10.1007/s00018-010-0335-5
Direito de acesso Acesso restrito
Tipo Resenha
Web of Science WOS:000277014300009
Endereço permanente http://repositorio.unifesp.br/handle/11600/32500

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