Indoleamine 2,3-dioxygenase (IDO) controls the fungal loads and cellular immunity in pulmonary paracoccidiodomycosis (PCM) developed by susceptible and resistant mice to the fungus (2010)
- Authors:
- Autor USP: CALICH, VERA LUCIA GARCIA - ICB
- Unidade: ICB
- Assunto: IMUNOLOGIA
- Language: Inglês
- Imprenta:
- Source:
- Título: Immunology Letters
- Volume/Número/Paginação/Ano: v. 22, suppl. 1 p. PP-092-15, 2010
- Conference titles: Internacional Congress of Mucosal Immunology Abstracts
-
ABNT
ARAUJO, E. F. e CALICH, V. L. G. Indoleamine 2,3-dioxygenase (IDO) controls the fungal loads and cellular immunity in pulmonary paracoccidiodomycosis (PCM) developed by susceptible and resistant mice to the fungus. Immunology Letters. Oxford: Instituto de Ciências Biomédicas, Universidade de São Paulo. . Acesso em: 11 mar. 2026. , 2010 -
APA
Araujo, E. F., & Calich, V. L. G. (2010). Indoleamine 2,3-dioxygenase (IDO) controls the fungal loads and cellular immunity in pulmonary paracoccidiodomycosis (PCM) developed by susceptible and resistant mice to the fungus. Immunology Letters. Oxford: Instituto de Ciências Biomédicas, Universidade de São Paulo. -
NLM
Araujo EF, Calich VLG. Indoleamine 2,3-dioxygenase (IDO) controls the fungal loads and cellular immunity in pulmonary paracoccidiodomycosis (PCM) developed by susceptible and resistant mice to the fungus. Immunology Letters. 2010 ; 22 suppl. 1 PP-092-15.[citado 2026 mar. 11 ] -
Vancouver
Araujo EF, Calich VLG. Indoleamine 2,3-dioxygenase (IDO) controls the fungal loads and cellular immunity in pulmonary paracoccidiodomycosis (PCM) developed by susceptible and resistant mice to the fungus. Immunology Letters. 2010 ; 22 suppl. 1 PP-092-15.[citado 2026 mar. 11 ] - 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
How to cite
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
