Regulation of parasite antigen-driven immune responses by interleukin-10 (IL-10) and IL-12 in lymphatic filariasis.
Identifieur interne : 004950 ( PubMed/Checkpoint ); précédent : 004949; suivant : 004951Regulation of parasite antigen-driven immune responses by interleukin-10 (IL-10) and IL-12 in lymphatic filariasis.
Auteurs : S. Mahanty [États-Unis] ; M. Ravichandran ; U. Raman ; K. Jayaraman ; V. Kumaraswami ; T B NutmanSource :
- Infection and immunity [ 0019-9567 ] ; 1997.
Descripteurs français
- KwdFr :
- Adolescent, Adulte, Adulte d'âge moyen, Agranulocytes (immunologie), Animaux, Anticorps bloquants (immunologie), Anticorps monoclonaux (immunologie), Antigènes d'helminthe (immunologie), Brugia malayi (immunologie), Division cellulaire, Femelle, Filariose lymphatique (immunologie), Humains, Interféron gamma (biosynthèse), Interleukine-10 (immunologie), Interleukine-12 (génétique), Interleukine-12 (immunologie), Interleukine-5 (immunologie), Lymphocytes T (cytologie), Lymphocytes T (immunologie), Lymphocytes auxiliaires Th1 (immunologie), Lymphocytes auxiliaires Th2 (immunologie), Mâle, Protéines recombinantes (immunologie), Régulation négative, Test ELISA, Tests de neutralisation, Tuberculine (immunologie).
- MESH :
- biosynthèse : Interféron gamma.
- cytologie : Lymphocytes T.
- génétique : Interleukine-12.
- immunologie : Agranulocytes, Anticorps bloquants, Anticorps monoclonaux, Antigènes d'helminthe, Brugia malayi, Filariose lymphatique, Interleukine-10, Interleukine-12, Interleukine-5, Lymphocytes T, Lymphocytes auxiliaires Th1, Lymphocytes auxiliaires Th2, Protéines recombinantes, Tuberculine.
- Adolescent, Adulte, Adulte d'âge moyen, Animaux, Division cellulaire, Femelle, Humains, Mâle, Régulation négative, Test ELISA, Tests de neutralisation.
English descriptors
- KwdEn :
- Adolescent, Adult, Animals, Antibodies, Blocking (immunology), Antibodies, Monoclonal (immunology), Antigens, Helminth (immunology), Brugia malayi (immunology), Cell Division, Down-Regulation, Elephantiasis, Filarial (immunology), Enzyme-Linked Immunosorbent Assay, Female, Humans, Interferon-gamma (biosynthesis), Interleukin-10 (immunology), Interleukin-12 (genetics), Interleukin-12 (immunology), Interleukin-5 (immunology), Leukocytes, Mononuclear (immunology), Male, Middle Aged, Neutralization Tests, Recombinant Proteins (immunology), T-Lymphocytes (cytology), T-Lymphocytes (immunology), Th1 Cells (immunology), Th2 Cells (immunology), Tuberculin (immunology).
- MESH :
- chemical , biosynthesis : Interferon-gamma.
- chemical , genetics : Interleukin-12.
- chemical , immunology : Antibodies, Blocking, Antibodies, Monoclonal, Antigens, Helminth, Interleukin-10, Interleukin-12, Interleukin-5, Recombinant Proteins, Tuberculin.
- cytology : T-Lymphocytes.
- immunology : Brugia malayi, Elephantiasis, Filarial, Leukocytes, Mononuclear, T-Lymphocytes, Th1 Cells, Th2 Cells.
- Adolescent, Adult, Animals, Cell Division, Down-Regulation, Enzyme-Linked Immunosorbent Assay, Female, Humans, Male, Middle Aged, Neutralization Tests.
Abstract
We investigated the mechanisms by which interleukin-10 (IL-10) regulates antigen-specific hyporesponsiveness in asymptomatic microfilaremic (MF) individuals. Peripheral blood mononuclear cells from MF individuals (n = 11) were stimulated in vitro with Brugia malayi antigen (BMA) or mycobacterial purified protein derivative (PPD) in the presence of neutralizing anti-IL-10 or isotype control monoclonal antibodies. As expected, BMA stimulated little or no gamma interferon (IFN-gamma) secretion in MF individuals, whereas PPD stimulated IFN-gamma in all but one. Neutralization of endogenous BMA-driven IL-10 secretion led to augmentation of IFN-gamma in seven of nine MF individuals (1.5- to 10-fold) and did so in a BMA-specific manner (PPD-driven IFN-gamma was augmented in only two of eight MF individuals and only 1.5- to 2-fold), indicating that IL-10 downregulates type 1 responses in these individuals. Type 2 responses (IL-5 secretion) were unaffected by the IL-10 blockade. To assess whether IL-12 could reverse the type 1 downregulation observed, the effect of recombinant human IL-12 (rhIL-12) on BMA-driven IL-5 and IFN-gamma production was also evaluated. rhIL-12 augmented both BMA- and PPD-driven IFN-gamma production 5- to 10-fold in six of nine MF individuals. These data demonstrate that IL-10 downregulates BMA-driven type 1 responses and that IL-12 can overcome downregulation of Th1 responses associated with MF but does so in a non-antigen-specific manner.
PubMed: 9125556
Affiliations:
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pubmed:9125556Le document en format XML
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Mahanty</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892</wicri:regionArea><wicri:noRegion>Maryland 20892</wicri:noRegion></affiliation></author><author><name sortKey="Ravichandran, M" sort="Ravichandran, M" uniqKey="Ravichandran M" first="M" last="Ravichandran">M. Ravichandran</name></author><author><name sortKey="Raman, U" sort="Raman, U" uniqKey="Raman U" first="U" last="Raman">U. Raman</name></author><author><name sortKey="Jayaraman, K" sort="Jayaraman, K" uniqKey="Jayaraman K" first="K" last="Jayaraman">K. Jayaraman</name></author><author><name sortKey="Kumaraswami, V" sort="Kumaraswami, V" uniqKey="Kumaraswami V" first="V" last="Kumaraswami">V. 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(immunology)</term><term>Interleukin-5 (immunology)</term><term>Leukocytes, Mononuclear (immunology)</term><term>Male</term><term>Middle Aged</term><term>Neutralization Tests</term><term>Recombinant Proteins (immunology)</term><term>T-Lymphocytes (cytology)</term><term>T-Lymphocytes (immunology)</term><term>Th1 Cells (immunology)</term><term>Th2 Cells (immunology)</term><term>Tuberculin (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adolescent</term><term>Adulte</term><term>Adulte d'âge moyen</term><term>Agranulocytes (immunologie)</term><term>Animaux</term><term>Anticorps bloquants (immunologie)</term><term>Anticorps monoclonaux (immunologie)</term><term>Antigènes d'helminthe (immunologie)</term><term>Brugia malayi (immunologie)</term><term>Division cellulaire</term><term>Femelle</term><term>Filariose lymphatique (immunologie)</term><term>Humains</term><term>Interféron gamma (biosynthèse)</term><term>Interleukine-10 (immunologie)</term><term>Interleukine-12 (génétique)</term><term>Interleukine-12 (immunologie)</term><term>Interleukine-5 (immunologie)</term><term>Lymphocytes T (cytologie)</term><term>Lymphocytes T (immunologie)</term><term>Lymphocytes auxiliaires Th1 (immunologie)</term><term>Lymphocytes auxiliaires Th2 (immunologie)</term><term>Mâle</term><term>Protéines recombinantes (immunologie)</term><term>Régulation négative</term><term>Test ELISA</term><term>Tests de neutralisation</term><term>Tuberculine (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Interferon-gamma</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interleukin-12</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Antibodies, Blocking</term><term>Antibodies, Monoclonal</term><term>Antigens, Helminth</term><term>Interleukin-10</term><term>Interleukin-12</term><term>Interleukin-5</term><term>Recombinant Proteins</term><term>Tuberculin</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Interféron gamma</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Lymphocytes T</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Interleukine-12</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Agranulocytes</term><term>Anticorps bloquants</term><term>Anticorps monoclonaux</term><term>Antigènes d'helminthe</term><term>Brugia malayi</term><term>Filariose lymphatique</term><term>Interleukine-10</term><term>Interleukine-12</term><term>Interleukine-5</term><term>Lymphocytes T</term><term>Lymphocytes auxiliaires Th1</term><term>Lymphocytes auxiliaires Th2</term><term>Protéines recombinantes</term><term>Tuberculine</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Brugia malayi</term><term>Elephantiasis, Filarial</term><term>Leukocytes, Mononuclear</term><term>T-Lymphocytes</term><term>Th1 Cells</term><term>Th2 Cells</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Animals</term><term>Cell Division</term><term>Down-Regulation</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Neutralization Tests</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adolescent</term><term>Adulte</term><term>Adulte d'âge moyen</term><term>Animaux</term><term>Division cellulaire</term><term>Femelle</term><term>Humains</term><term>Mâle</term><term>Régulation négative</term><term>Test ELISA</term><term>Tests de neutralisation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We investigated the mechanisms by which interleukin-10 (IL-10) regulates antigen-specific hyporesponsiveness in asymptomatic microfilaremic (MF) individuals. Peripheral blood mononuclear cells from MF individuals (n = 11) were stimulated in vitro with Brugia malayi antigen (BMA) or mycobacterial purified protein derivative (PPD) in the presence of neutralizing anti-IL-10 or isotype control monoclonal antibodies. As expected, BMA stimulated little or no gamma interferon (IFN-gamma) secretion in MF individuals, whereas PPD stimulated IFN-gamma in all but one. Neutralization of endogenous BMA-driven IL-10 secretion led to augmentation of IFN-gamma in seven of nine MF individuals (1.5- to 10-fold) and did so in a BMA-specific manner (PPD-driven IFN-gamma was augmented in only two of eight MF individuals and only 1.5- to 2-fold), indicating that IL-10 downregulates type 1 responses in these individuals. Type 2 responses (IL-5 secretion) were unaffected by the IL-10 blockade. To assess whether IL-12 could reverse the type 1 downregulation observed, the effect of recombinant human IL-12 (rhIL-12) on BMA-driven IL-5 and IFN-gamma production was also evaluated. rhIL-12 augmented both BMA- and PPD-driven IFN-gamma production 5- to 10-fold in six of nine MF individuals. These data demonstrate that IL-10 downregulates BMA-driven type 1 responses and that IL-12 can overcome downregulation of Th1 responses associated with MF but does so in a non-antigen-specific manner.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9125556</PMID><DateCreated><Year>1997</Year><Month>05</Month><Day>15</Day></DateCreated><DateCompleted><Year>1997</Year><Month>05</Month><Day>15</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0019-9567</ISSN><JournalIssue CitedMedium="Print"><Volume>65</Volume><Issue>5</Issue><PubDate><Year>1997</Year><Month>May</Month></PubDate></JournalIssue><Title>Infection and immunity</Title><ISOAbbreviation>Infect. Immun.</ISOAbbreviation></Journal><ArticleTitle>Regulation of parasite antigen-driven immune responses by interleukin-10 (IL-10) and IL-12 in lymphatic filariasis.</ArticleTitle><Pagination><MedlinePgn>1742-7</MedlinePgn></Pagination><Abstract><AbstractText>We investigated the mechanisms by which interleukin-10 (IL-10) regulates antigen-specific hyporesponsiveness in asymptomatic microfilaremic (MF) individuals. Peripheral blood mononuclear cells from MF individuals (n = 11) were stimulated in vitro with Brugia malayi antigen (BMA) or mycobacterial purified protein derivative (PPD) in the presence of neutralizing anti-IL-10 or isotype control monoclonal antibodies. As expected, BMA stimulated little or no gamma interferon (IFN-gamma) secretion in MF individuals, whereas PPD stimulated IFN-gamma in all but one. Neutralization of endogenous BMA-driven IL-10 secretion led to augmentation of IFN-gamma in seven of nine MF individuals (1.5- to 10-fold) and did so in a BMA-specific manner (PPD-driven IFN-gamma was augmented in only two of eight MF individuals and only 1.5- to 2-fold), indicating that IL-10 downregulates type 1 responses in these individuals. Type 2 responses (IL-5 secretion) were unaffected by the IL-10 blockade. To assess whether IL-12 could reverse the type 1 downregulation observed, the effect of recombinant human IL-12 (rhIL-12) on BMA-driven IL-5 and IFN-gamma production was also evaluated. rhIL-12 augmented both BMA- and PPD-driven IFN-gamma production 5- to 10-fold in six of nine MF individuals. These data demonstrate that IL-10 downregulates BMA-driven type 1 responses and that IL-12 can overcome downregulation of Th1 responses associated with MF but does so in a non-antigen-specific manner.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mahanty</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ravichandran</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Raman</LastName><ForeName>U</ForeName><Initials>U</Initials></Author><Author ValidYN="Y"><LastName>Jayaraman</LastName><ForeName>K</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Kumaraswami</LastName><ForeName>V</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Nutman</LastName><ForeName>T B</ForeName><Initials>TB</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Infect Immun</MedlineTA><NlmUniqueID>0246127</NlmUniqueID><ISSNLinking>0019-9567</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019138">Antibodies, Blocking</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000911">Antibodies, Monoclonal</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000947">Antigens, Helminth</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015848">Interleukin-5</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011994">Recombinant Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014373">Tuberculin</NameOfSubstance></Chemical><Chemical><RegistryNumber>130068-27-8</RegistryNumber><NameOfSubstance UI="D016753">Interleukin-10</NameOfSubstance></Chemical><Chemical><RegistryNumber>187348-17-0</RegistryNumber><NameOfSubstance UI="D018664">Interleukin-12</NameOfSubstance></Chemical><Chemical><RegistryNumber>82115-62-6</RegistryNumber><NameOfSubstance UI="D007371">Interferon-gamma</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CitationSubset>X</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>J Exp Med. 1996 Jul 1;184(1):19-29</RefSource><PMID Version="1">8691133</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Immunol. 1993 Sep 15;151(6):3192-8</RefSource><PMID Version="1">8376775</PMID></CommentsCorrections><CommentsCorrections 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MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018417" MajorTopicYN="N">Th1 Cells</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018418" MajorTopicYN="N">Th2 Cells</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014373" MajorTopicYN="N">Tuberculin</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC175209</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1997</Year><Month>5</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1997</Year><Month>5</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1997</Year><Month>5</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9125556</ArticleId><ArticleId IdType="pmc">PMC175209</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Jayaraman, K" sort="Jayaraman, K" uniqKey="Jayaraman K" first="K" last="Jayaraman">K. Jayaraman</name><name sortKey="Kumaraswami, V" sort="Kumaraswami, V" uniqKey="Kumaraswami V" first="V" last="Kumaraswami">V. Kumaraswami</name><name sortKey="Nutman, T B" sort="Nutman, T B" uniqKey="Nutman T" first="T B" last="Nutman">T B Nutman</name><name sortKey="Raman, U" sort="Raman, U" uniqKey="Raman U" first="U" last="Raman">U. Raman</name><name sortKey="Ravichandran, M" sort="Ravichandran, M" uniqKey="Ravichandran M" first="M" last="Ravichandran">M. Ravichandran</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Mahanty, S" sort="Mahanty, S" uniqKey="Mahanty S" first="S" last="Mahanty">S. Mahanty</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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