Susceptible and resistant mice to P. Brasiliensis infection use an indoleamine 2,3-dioxygenase mechanism to control fungal growth (2008)
- Authors:
- Autor USP: CALICH, VERA LUCIA GARCIA - ICB
- Unidade: ICB
- Assunto: IMUNOLOGIA
- Language: Inglês
- Imprenta:
- Publisher place: Ribeirão Preto
- Date published: 2008
- Source:
- Título: Resumos
- Conference titles: Congress of the Brazilian Society for Immunology - SBI
-
ABNT
ARAUJO, Eliseu Frank de e CALICH, Vera Lúcia Garcia. Susceptible and resistant mice to P. Brasiliensis infection use an indoleamine 2,3-dioxygenase mechanism to control fungal growth. 2008, Anais.. Ribeirão Preto: Instituto de Ciências Biomédicas, Universidade de São Paulo, 2008. . Acesso em: 17 mar. 2026. -
APA
Araujo, E. F. de, & Calich, V. L. G. (2008). Susceptible and resistant mice to P. Brasiliensis infection use an indoleamine 2,3-dioxygenase mechanism to control fungal growth. In Resumos. Ribeirão Preto: Instituto de Ciências Biomédicas, Universidade de São Paulo. -
NLM
Araujo EF de, Calich VLG. Susceptible and resistant mice to P. Brasiliensis infection use an indoleamine 2,3-dioxygenase mechanism to control fungal growth. Resumos. 2008 ;[citado 2026 mar. 17 ] -
Vancouver
Araujo EF de, Calich VLG. Susceptible and resistant mice to P. Brasiliensis infection use an indoleamine 2,3-dioxygenase mechanism to control fungal growth. Resumos. 2008 ;[citado 2026 mar. 17 ] - cd28 costimulatory molecule deficiency in more severe paracoccidioides brasiliensis infection but protects mice from life-threatening immunopathology
- Paracoccidioides brasiliensis infection determines dentric cells to diferentiate to the plasmacytoid subpopulation which induces a more severe pulmonary infection when transfered to resistant mice
- The IDO-AhR axis controls Th17/Treg immunity in a pulmonary model of fungal infection
- TLR-2 is a negative regulator of TH17 cells and tissue pathology in a pulmonary model of fungal infection
- Absence of TLR2 results in less severe paracoccidioidomycosis but increased inflammatory response caused by PMN & TH17 cells
- Toll like receptors and the adaptor molecule MYD88 play an important role in pulmonary paracoccidioidomycosis
- TLR2 is a negative regulator of Th17 cells and tissue pathology in a pulmonary model of fungal infection
- Human alfa / beta and gama / delta t cells respond to proteins of the yeast form of paracoccidioides brasiliensis
- The immune response of high (H) and low responders (L) mice (selection III) and F1 (HIII x LIII) hybrids to paracoccidioides brasiliensis infection
- PMN leukocytes play a more prominent role in natural immunity of susceptible than resistant mice to pulmonary paracoccidiodomycosis
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