Co-adsorption of allergen with bacterial lipopolysaccharide to Alum suppresses the development of allergic asthma signaling through Toll like receptor 4 and the adaptor molecule MyD88 (2007)
- Authors:
- Autor USP: RUSSO, MOMTCHILO - ICB
- Unidade: ICB
- Assunto: IMUNOLOGIA
- Language: Inglês
- Imprenta:
- Publisher: Sociedade Brasileira de Imunologia
- Publisher place: Rio de Janeiro
- Date published: 2007
- Source:
- Título: Abstracts
- Conference titles: International Congress of Immunology
-
ABNT
BORTOLATTO, J. et al. Co-adsorption of allergen with bacterial lipopolysaccharide to Alum suppresses the development of allergic asthma signaling through Toll like receptor 4 and the adaptor molecule MyD88. 2007, Anais.. Rio de Janeiro: Sociedade Brasileira de Imunologia, 2007. . Acesso em: 04 mar. 2026. -
APA
Bortolatto, J., Rodriguez, D., Keller, A., Faquim-Mauro, E., Borducchi, E., Bastos, K., et al. (2007). Co-adsorption of allergen with bacterial lipopolysaccharide to Alum suppresses the development of allergic asthma signaling through Toll like receptor 4 and the adaptor molecule MyD88. In Abstracts. Rio de Janeiro: Sociedade Brasileira de Imunologia. -
NLM
Bortolatto J, Rodriguez D, Keller A, Faquim-Mauro E, Borducchi E, Bastos K, Candrian S, Schnyder B, Ryffel B, Russo M. Co-adsorption of allergen with bacterial lipopolysaccharide to Alum suppresses the development of allergic asthma signaling through Toll like receptor 4 and the adaptor molecule MyD88. Abstracts. 2007 ;[citado 2026 mar. 04 ] -
Vancouver
Bortolatto J, Rodriguez D, Keller A, Faquim-Mauro E, Borducchi E, Bastos K, Candrian S, Schnyder B, Ryffel B, Russo M. Co-adsorption of allergen with bacterial lipopolysaccharide to Alum suppresses the development of allergic asthma signaling through Toll like receptor 4 and the adaptor molecule MyD88. Abstracts. 2007 ;[citado 2026 mar. 04 ] - Dissociation between airway hyperresponsiveness and acute physiological response to allergen inhalation in mice selected for maximum (AIRmax) or minimum (AIRmin) acute inflammatory response
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