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Provedor de dados:  BJMBR
País:  Brazil
Título:  Interleukin-12 and protective immunity to schistosomes
Autores:  Mountford,A.P.
Shires,V.L.
Anderson,S.
Data:  1998-01-01
Ano:  1998
Palavras-chave:  Schistosoma
Interleukin-12
Adjuvant
Vaccine
Th1
Resumo:  The attenuated vaccine against Schistosoma mansoni induces Th1-mediated protective immunity and we have sought to identify a role for IL-12 in this model. Elevated levels of IL-12 (p40 mRNA) were detected in the lymph nodes (LN) and the lungs of vaccinated mice, whilst treatment of vaccinated mice with anti-IL-12 antibodies decreased the ratio of IFN<FONT FACE="Symbol">g</font>:IL-4 secreted by in vitro-cultured LN cells. However, there was only marginal abrogation of the level of resistance in these mice. Soluble antigens from the lung-stage of the parasite (SLAP) appeared to be efficient stimulators of IFN<FONT FACE="Symbol">g</font> and IL-12 secretion. These antigens when used to immunise mice in conjunction with IL-12 as an adjuvant, elicited a polarised Th1 response with abundant IFN<FONT FACE="Symbol">g</font> secretion but no IL-4. This immunisation regime also induced significant protection against reinfection, whereas inoculation of mice with SLAP alone did not. The induction of a dominant Th1 response using SLAP + IL-12 probably operates via IFN<FONT FACE="Symbol">g</font> production by natural killer (NK) cells stimulated by IL-12, since in vivo ablation of NK cells using anti-NK1.1 antibody reduced CD4+-dependent IFN<FONT FACE="Symbol">g</font> production from cultured LN cells by over 97%. Nevertheless, in mice with a genetic disruption of the IFN<FONT FACE="Symbol">g</font> receptor, administration of SLAP + IL-12 induced levels of IFN<FONT FACE="Symbol">g</font> equal to those in wild-type mice, thus showing that in this model IL-12 can directly prime T cells independent of IFN<FONT FACE="Symbol">g</font>. Clearly, IL-12 has a critical role in protective immunity to schistosomes and it may aid the development of an effective vaccine against this disease
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1998000100023
Editor:  Associação Brasileira de Divulgação Científica
Relação:  10.1590/S0100-879X1998000100023
Formato:  text/html
Fonte:  Brazilian Journal of Medical and Biological Research v.31 n.1 1998
Direitos:  info:eu-repo/semantics/openAccess
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