Interferon gamma is a key cytokine in lung phase immunity to schistosomes but what is its precise role?
Autor(a) principal: | |
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Data de Publicação: | 1998 |
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=S0100-879X1998000100022 |
Resumo: | Vaccination of mice with radiation-attenuated cercariae of Schistosoma mansoni induces a high level of protection against challenge with normal larvae. The immune effector mechanism, which operates in the lungs, is a cell-mediated delayed-type hypersensitivity response and involves the formation of a tight focus of mononuclear cells around embolised larvae. CD4+ T cells with Th1 characteristics are a major component of the infiltrate. They secrete abundant interferon gamma (IFN<FONT FACE="Symbol">g</font>) upon antigen stimulation in vitro, whilst in vivo neutralisation of the cytokine results in 90% abrogation of immunity. IFN<FONT FACE="Symbol">g</font> can induce a large number of genes and an attempt has been made to identify the ones which are essential components of the effector mechanism. Inducible nitric oxide synthase (iNOS) is such a candidate and nitric oxide (NO) is produced by cultures of airway leucocytes from the lungs of vaccinated mice post-challenge. However, the continued resistance of mice with a disrupted iNOS gene indicates that NO has only a minor role in the protective response. Mice with a disrupted IFN<FONT FACE="Symbol">g</font> receptor gene have been used to dissect the role of the cytokine. After vaccination and challenge, CD4+ T cells from the pulmonary interstitium have reduced levels of ICAM-1 and LFA-1 expression, compared to wild-type animals, which coincides with a reduced cohesiveness of foci. However, immunity is not significantly impaired in mice with a disrupted ICAM-1 gene, and focus formation is normal. Similarly, a role has not been found for CD2/CD48 interactions in cell aggregation. Possible IFN<FONT FACE="Symbol">g</font>-inducible molecules yet to be fully investigated include other ligand-receptor pairs, chemokines, and tumour necrosis factor <FONT FACE="Symbol">a</font>. |
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Brazilian Journal of Medical and Biological Research |
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Interferon gamma is a key cytokine in lung phase immunity to schistosomes but what is its precise role?interferon gammaSchistosoma mansonilung phase immunitynitric oxideadhesion moleculeVaccination of mice with radiation-attenuated cercariae of Schistosoma mansoni induces a high level of protection against challenge with normal larvae. The immune effector mechanism, which operates in the lungs, is a cell-mediated delayed-type hypersensitivity response and involves the formation of a tight focus of mononuclear cells around embolised larvae. CD4+ T cells with Th1 characteristics are a major component of the infiltrate. They secrete abundant interferon gamma (IFN<FONT FACE="Symbol">g</font>) upon antigen stimulation in vitro, whilst in vivo neutralisation of the cytokine results in 90% abrogation of immunity. IFN<FONT FACE="Symbol">g</font> can induce a large number of genes and an attempt has been made to identify the ones which are essential components of the effector mechanism. Inducible nitric oxide synthase (iNOS) is such a candidate and nitric oxide (NO) is produced by cultures of airway leucocytes from the lungs of vaccinated mice post-challenge. However, the continued resistance of mice with a disrupted iNOS gene indicates that NO has only a minor role in the protective response. Mice with a disrupted IFN<FONT FACE="Symbol">g</font> receptor gene have been used to dissect the role of the cytokine. After vaccination and challenge, CD4+ T cells from the pulmonary interstitium have reduced levels of ICAM-1 and LFA-1 expression, compared to wild-type animals, which coincides with a reduced cohesiveness of foci. However, immunity is not significantly impaired in mice with a disrupted ICAM-1 gene, and focus formation is normal. Similarly, a role has not been found for CD2/CD48 interactions in cell aggregation. Possible IFN<FONT FACE="Symbol">g</font>-inducible molecules yet to be fully investigated include other ligand-receptor pairs, chemokines, and tumour necrosis factor <FONT FACE="Symbol">a</font>.Associação Brasileira de Divulgação Científica1998-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1998000100022Brazilian 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/S0100-879X1998000100022info:eu-repo/semantics/openAccessWilson,R.A.eng1998-10-07T00:00:00Zoai:scielo:S0100-879X1998000100022Revistahttps://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 |
Interferon gamma is a key cytokine in lung phase immunity to schistosomes but what is its precise role? |
title |
Interferon gamma is a key cytokine in lung phase immunity to schistosomes but what is its precise role? |
spellingShingle |
Interferon gamma is a key cytokine in lung phase immunity to schistosomes but what is its precise role? Wilson,R.A. interferon gamma Schistosoma mansoni lung phase immunity nitric oxide adhesion molecule |
title_short |
Interferon gamma is a key cytokine in lung phase immunity to schistosomes but what is its precise role? |
title_full |
Interferon gamma is a key cytokine in lung phase immunity to schistosomes but what is its precise role? |
title_fullStr |
Interferon gamma is a key cytokine in lung phase immunity to schistosomes but what is its precise role? |
title_full_unstemmed |
Interferon gamma is a key cytokine in lung phase immunity to schistosomes but what is its precise role? |
title_sort |
Interferon gamma is a key cytokine in lung phase immunity to schistosomes but what is its precise role? |
author |
Wilson,R.A. |
author_facet |
Wilson,R.A. |
author_role |
author |
dc.contributor.author.fl_str_mv |
Wilson,R.A. |
dc.subject.por.fl_str_mv |
interferon gamma Schistosoma mansoni lung phase immunity nitric oxide adhesion molecule |
topic |
interferon gamma Schistosoma mansoni lung phase immunity nitric oxide adhesion molecule |
description |
Vaccination of mice with radiation-attenuated cercariae of Schistosoma mansoni induces a high level of protection against challenge with normal larvae. The immune effector mechanism, which operates in the lungs, is a cell-mediated delayed-type hypersensitivity response and involves the formation of a tight focus of mononuclear cells around embolised larvae. CD4+ T cells with Th1 characteristics are a major component of the infiltrate. They secrete abundant interferon gamma (IFN<FONT FACE="Symbol">g</font>) upon antigen stimulation in vitro, whilst in vivo neutralisation of the cytokine results in 90% abrogation of immunity. IFN<FONT FACE="Symbol">g</font> can induce a large number of genes and an attempt has been made to identify the ones which are essential components of the effector mechanism. Inducible nitric oxide synthase (iNOS) is such a candidate and nitric oxide (NO) is produced by cultures of airway leucocytes from the lungs of vaccinated mice post-challenge. However, the continued resistance of mice with a disrupted iNOS gene indicates that NO has only a minor role in the protective response. Mice with a disrupted IFN<FONT FACE="Symbol">g</font> receptor gene have been used to dissect the role of the cytokine. After vaccination and challenge, CD4+ T cells from the pulmonary interstitium have reduced levels of ICAM-1 and LFA-1 expression, compared to wild-type animals, which coincides with a reduced cohesiveness of foci. However, immunity is not significantly impaired in mice with a disrupted ICAM-1 gene, and focus formation is normal. Similarly, a role has not been found for CD2/CD48 interactions in cell aggregation. Possible IFN<FONT FACE="Symbol">g</font>-inducible molecules yet to be fully investigated include other ligand-receptor pairs, chemokines, and tumour necrosis factor <FONT FACE="Symbol">a</font>. |
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=S0100-879X1998000100022 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1998000100022 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/S0100-879X1998000100022 |
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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1754302929168236544 |