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Utilize este identificador para citar ou criar um link para este item: http://acervodigital.unesp.br/handle/11449/112632
Título: 
BCG and BCG/DNAhsp65 Vaccinations Promote Protective Effects without Deleterious Consequences for Experimental Autoimmune Encephalomyelitis
Autor(es): 
Instituição: 
  • Universidade Estadual Paulista (UNESP)
  • Universidade de São Paulo (USP)
ISSN: 
1740-2522
Financiador: 
  • Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
  • Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Número do financiamento: 
  • FAPESP: 07/05353-8
  • CNPq: 473351/2004-8
Resumo: 
A prime-boost strategy conserving BCG is considered the most promising vaccine to control tuberculosis. A boost with a DNA vaccine containing the mycobacterial gene of a heat shock protein (pVAXhsp65) after BCG priming protected mice against experimental tuberculosis. However, anti-hsp65 immunity could worsen an autoimmune disease due to molecular mimicry. In this investigation, we evaluated the effect of a previous BCG or BCG/pVAXhsp65 immunization on experimental autoimmune encephalomyelitis (EAE) development. Female Lewis rats were immunized with BCG or BCG followed by pVAXhsp65 boosters. The animals underwent EAE induction and were daily evaluated for weight loss and clinical score. They were euthanized during recovery phase to assess immune response and inflammatory infiltration at the central nervous system. Previous immunization did not aggravate or accelerate clinical score or weight loss. In addition, this procedure clearly decreased inflammation in the brain. BCG immunization modulated the host immune response by triggering a significant reduction in IL-10 and IFN-gamma levels induced by myelin basic protein. These data indicated that vaccination protocols with BCG or BCG followed by boosters with pVAXhsp65 did not trigger a deleterious effect on EAE evolution.
Data de publicação: 
1-Jan-2013
Citação: 
Clinical & Developmental Immunology. New York: Hindawi Publishing Corporation, 9 p., 2013.
Duração: 
9
Publicador: 
Hindawi Publishing Corporation
Fonte: 
http://dx.doi.org/10.1155/2013/721383
Endereço permanente: 
Direitos de acesso: 
Acesso aberto
Tipo: 
outro
Fonte completa:
http://repositorio.unesp.br/handle/11449/112632
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