Nod-like receptors-dependent innate immune responses to intracellular pathogens (2011)
- Autor:
- Autor USP: ZAMBONI, DARIO SIMÕES - FMRP
- Unidade: FMRP
- Subjects: INFECÇÕES BACTERIANAS; RECEPTORES
- Language: Inglês
- Imprenta:
- Source:
- Título do periódico: Programa
- Conference titles: Reunião Anual da Federação de Sociedades de Biologia Experimental (FeSBE)
-
ABNT
ZAMBONI, Dario Simões. Nod-like receptors-dependent innate immune responses to intracellular pathogens. 2011, Anais.. São Paulo: FeSBE, 2011. . Acesso em: 24 abr. 2024. -
APA
Zamboni, D. S. (2011). Nod-like receptors-dependent innate immune responses to intracellular pathogens. In Programa. São Paulo: FeSBE. -
NLM
Zamboni DS. Nod-like receptors-dependent innate immune responses to intracellular pathogens. Programa. 2011 ;[citado 2024 abr. 24 ] -
Vancouver
Zamboni DS. Nod-like receptors-dependent innate immune responses to intracellular pathogens. Programa. 2011 ;[citado 2024 abr. 24 ] - Role of inflammasomes in diffuse and localized cutaneous Leishmaniasis
- Autophagy downstream of endosomal Toll-like receptor signaling in macrophages is a key mechanism for resistance to Leishmania major infection
- Role of the transcriptional regulator SP140 in resistance to bacterial infections via repression of type I interferons
- Unique role of the Nlrc4 inflammasome for pore formation and pyroptosis in response to flagellated bacterial pathogens
- NALP3: a key player in caspase-1 activation
- NOD1 and NOD2 signaling in infection and inflammation
- Participação dos receptores de reconhecimento padrão NOD1 e NOD2 no recrutamento de neutrófilos para o pulmão em resposta a infecção murina por legionella penumophila
- Critical role of ASC inflammasomes and bacterial type IV secretion system in caspase-1 activation and host innate resistance to Brucella abortus infection
- Inflammasome mediated innate immune responses to Leishmania
- Inhibition of non-canonical inflammasome activation in response to Legionella pneumophila by a Dot/Icm effector of Coxiella burnetii
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