Interleukin-12 and protective immunity to schistosomes
Autor(a) principal: | |
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Data de Publicação: | 1998 |
Outros Autores: | , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Brazilian Journal of Medical and Biological Research |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1998000100023 |
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 |
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Brazilian Journal of Medical and Biological Research |
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Interleukin-12 and protective immunity to schistosomesSchistosomainterleukin-12adjuvantvaccineTh1The 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 diseaseAssociação Brasileira de Divulgação Científica1998-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1998000100023Brazilian Journal of Medical and Biological Research v.31 n.1 1998reponame:Brazilian Journal of Medical and Biological Researchinstname:Associação Brasileira de Divulgação Científica (ABDC)instacron:ABDC10.1590/S0100-879X1998000100023info:eu-repo/semantics/openAccessMountford,A.P.Shires,V.L.Anderson,S.eng1998-10-07T00:00:00Zoai:scielo:S0100-879X1998000100023Revistahttps://www.bjournal.org/https://old.scielo.br/oai/scielo-oai.phpbjournal@terra.com.br||bjournal@terra.com.br1414-431X0100-879Xopendoar:1998-10-07T00:00Brazilian Journal of Medical and Biological Research - Associação Brasileira de Divulgação Científica (ABDC)false |
dc.title.none.fl_str_mv |
Interleukin-12 and protective immunity to schistosomes |
title |
Interleukin-12 and protective immunity to schistosomes |
spellingShingle |
Interleukin-12 and protective immunity to schistosomes Mountford,A.P. Schistosoma interleukin-12 adjuvant vaccine Th1 |
title_short |
Interleukin-12 and protective immunity to schistosomes |
title_full |
Interleukin-12 and protective immunity to schistosomes |
title_fullStr |
Interleukin-12 and protective immunity to schistosomes |
title_full_unstemmed |
Interleukin-12 and protective immunity to schistosomes |
title_sort |
Interleukin-12 and protective immunity to schistosomes |
author |
Mountford,A.P. |
author_facet |
Mountford,A.P. Shires,V.L. Anderson,S. |
author_role |
author |
author2 |
Shires,V.L. Anderson,S. |
author2_role |
author author |
dc.contributor.author.fl_str_mv |
Mountford,A.P. Shires,V.L. Anderson,S. |
dc.subject.por.fl_str_mv |
Schistosoma interleukin-12 adjuvant vaccine Th1 |
topic |
Schistosoma interleukin-12 adjuvant vaccine Th1 |
description |
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 |
publishDate |
1998 |
dc.date.none.fl_str_mv |
1998-01-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1998000100023 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1998000100023 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/S0100-879X1998000100023 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Associação Brasileira de Divulgação Científica |
publisher.none.fl_str_mv |
Associação Brasileira de Divulgação Científica |
dc.source.none.fl_str_mv |
Brazilian Journal of Medical and Biological Research v.31 n.1 1998 reponame:Brazilian Journal of Medical and Biological Research instname:Associação Brasileira de Divulgação Científica (ABDC) instacron:ABDC |
instname_str |
Associação Brasileira de Divulgação Científica (ABDC) |
instacron_str |
ABDC |
institution |
ABDC |
reponame_str |
Brazilian Journal of Medical and Biological Research |
collection |
Brazilian Journal of Medical and Biological Research |
repository.name.fl_str_mv |
Brazilian Journal of Medical and Biological Research - Associação Brasileira de Divulgação Científica (ABDC) |
repository.mail.fl_str_mv |
bjournal@terra.com.br||bjournal@terra.com.br |
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1754302929170333696 |