Regulation of parasite antigen-induced T cell growth factor activity and proliferative responsiveness in Brugia pahangi-infected jirds.
Identifieur interne : 005744 ( PubMed/Checkpoint ); précédent : 005743; suivant : 005745Regulation of parasite antigen-induced T cell growth factor activity and proliferative responsiveness in Brugia pahangi-infected jirds.
Auteurs : L E Leiva ; P J LammieSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 0022-1767 ] ; 1989.
Descripteurs français
- KwdFr :
- Activation des lymphocytes, Animaux, Antigènes d'helminthe (immunologie), Brugia (immunologie), Cinétique, Filariose lymphatique (immunologie), Filarioses (immunologie), Gerbillinae, Interleukine-2 (biosynthèse), Interleukine-2 (pharmacologie), Lymphocytes T (immunologie), Microfilaria (immunologie), Mâle, Noeuds lymphatiques (immunologie), Rate (immunologie).
- MESH :
- biosynthèse : Interleukine-2.
- immunologie : Antigènes d'helminthe, Brugia, Filariose lymphatique, Filarioses, Lymphocytes T, Microfilaria, Noeuds lymphatiques, Rate.
- pharmacologie : Interleukine-2.
- Activation des lymphocytes, Animaux, Cinétique, Gerbillinae, Mâle.
English descriptors
- KwdEn :
- Animals, Antigens, Helminth (immunology), Brugia (immunology), Elephantiasis, Filarial (immunology), Filariasis (immunology), Gerbillinae, Interleukin-2 (biosynthesis), Interleukin-2 (pharmacology), Kinetics, Lymph Nodes (immunology), Lymphocyte Activation, Male, Microfilariae (immunology), Spleen (immunology), T-Lymphocytes (immunology).
- MESH :
- chemical , biosynthesis : Interleukin-2.
- chemical , immunology : Antigens, Helminth.
- immunology : Brugia, Elephantiasis, Filarial, Filariasis, Lymph Nodes, Microfilariae, Spleen, T-Lymphocytes.
- chemical , pharmacology : Interleukin-2.
- Animals, Gerbillinae, Kinetics, Lymphocyte Activation, Male.
Abstract
Previous studies have demonstrated that the induction of immunoregulatory mechanisms in the spleens of Brugia pahangi-infected jirds is correlated with the onset of microfilaremia. This study investigated the relationship between production of a factor with IL-2-like activity and the regulation of T cell-mediated responses in jirds experimentally infected with B. pahangi. A factor present in culture supernatants of mitogen-stimulated jird lymphocytes supported the proliferation of murine CTLL cells and provided the basis for an IL-2 assay. Mitogen induced proliferative responses and IL-2 production of spleen cells but not lymph node cells from pre-patent and microfilaremic jirds were suppressed. Both B. pahangi Ag-induced proliferative responsiveness and IL-2 production of spleen cells from microfilaremic jirds were also suppressed relative to lymph node cells from the same animals or spleen cells from B. pahangi immunized or prepatent jirds. Depletion of histamine receptor-bearing cells restored the ability of spleen cells from microfilaremic jirds to produce significant levels of IL-2. In addition, in add-mixture experiments, spleen cells from microfilaremic jirds suppressed Ag-induced IL-2 production by cells from either B. pahangi- or KHL-immunized jirds. Exogenous IL-2 failed to reconstitute the suppressed Ag-induced proliferative response of spleen cells from microfilaremic jirds. This study demonstrates that the down-regulation of immune responses in B. pahangi infection is a cell-mediated event and is associated with an inability to produce IL-2.
PubMed: 2783709
Affiliations:
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Lammie</name></author></analytic><series><title level="j">Journal of immunology (Baltimore, Md. : 1950)</title><idno type="ISSN">0022-1767</idno><imprint><date when="1989" type="published">1989</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antigens, Helminth (immunology)</term><term>Brugia (immunology)</term><term>Elephantiasis, Filarial (immunology)</term><term>Filariasis (immunology)</term><term>Gerbillinae</term><term>Interleukin-2 (biosynthesis)</term><term>Interleukin-2 (pharmacology)</term><term>Kinetics</term><term>Lymph Nodes (immunology)</term><term>Lymphocyte Activation</term><term>Male</term><term>Microfilariae (immunology)</term><term>Spleen (immunology)</term><term>T-Lymphocytes (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Activation des lymphocytes</term><term>Animaux</term><term>Antigènes d'helminthe (immunologie)</term><term>Brugia (immunologie)</term><term>Cinétique</term><term>Filariose lymphatique (immunologie)</term><term>Filarioses (immunologie)</term><term>Gerbillinae</term><term>Interleukine-2 (biosynthèse)</term><term>Interleukine-2 (pharmacologie)</term><term>Lymphocytes T (immunologie)</term><term>Microfilaria (immunologie)</term><term>Mâle</term><term>Noeuds lymphatiques (immunologie)</term><term>Rate (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Interleukin-2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Antigens, Helminth</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Interleukine-2</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Antigènes d'helminthe</term><term>Brugia</term><term>Filariose lymphatique</term><term>Filarioses</term><term>Lymphocytes T</term><term>Microfilaria</term><term>Noeuds lymphatiques</term><term>Rate</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Brugia</term><term>Elephantiasis, Filarial</term><term>Filariasis</term><term>Lymph Nodes</term><term>Microfilariae</term><term>Spleen</term><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Interleukine-2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Interleukin-2</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Gerbillinae</term><term>Kinetics</term><term>Lymphocyte Activation</term><term>Male</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Activation des lymphocytes</term><term>Animaux</term><term>Cinétique</term><term>Gerbillinae</term><term>Mâle</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Previous studies have demonstrated that the induction of immunoregulatory mechanisms in the spleens of Brugia pahangi-infected jirds is correlated with the onset of microfilaremia. This study investigated the relationship between production of a factor with IL-2-like activity and the regulation of T cell-mediated responses in jirds experimentally infected with B. pahangi. A factor present in culture supernatants of mitogen-stimulated jird lymphocytes supported the proliferation of murine CTLL cells and provided the basis for an IL-2 assay. Mitogen induced proliferative responses and IL-2 production of spleen cells but not lymph node cells from pre-patent and microfilaremic jirds were suppressed. Both B. pahangi Ag-induced proliferative responsiveness and IL-2 production of spleen cells from microfilaremic jirds were also suppressed relative to lymph node cells from the same animals or spleen cells from B. pahangi immunized or prepatent jirds. Depletion of histamine receptor-bearing cells restored the ability of spleen cells from microfilaremic jirds to produce significant levels of IL-2. In addition, in add-mixture experiments, spleen cells from microfilaremic jirds suppressed Ag-induced IL-2 production by cells from either B. pahangi- or KHL-immunized jirds. Exogenous IL-2 failed to reconstitute the suppressed Ag-induced proliferative response of spleen cells from microfilaremic jirds. This study demonstrates that the down-regulation of immune responses in B. pahangi infection is a cell-mediated event and is associated with an inability to produce IL-2.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">2783709</PMID><DateCreated><Year>1989</Year><Month>03</Month><Day>13</Day></DateCreated><DateCompleted><Year>1989</Year><Month>03</Month><Day>13</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>23</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-1767</ISSN><JournalIssue CitedMedium="Print"><Volume>142</Volume><Issue>4</Issue><PubDate><Year>1989</Year><Month>Feb</Month><Day>15</Day></PubDate></JournalIssue><Title>Journal of immunology (Baltimore, Md. : 1950)</Title><ISOAbbreviation>J. Immunol.</ISOAbbreviation></Journal><ArticleTitle>Regulation of parasite antigen-induced T cell growth factor activity and proliferative responsiveness in Brugia pahangi-infected jirds.</ArticleTitle><Pagination><MedlinePgn>1304-9</MedlinePgn></Pagination><Abstract><AbstractText>Previous studies have demonstrated that the induction of immunoregulatory mechanisms in the spleens of Brugia pahangi-infected jirds is correlated with the onset of microfilaremia. This study investigated the relationship between production of a factor with IL-2-like activity and the regulation of T cell-mediated responses in jirds experimentally infected with B. pahangi. A factor present in culture supernatants of mitogen-stimulated jird lymphocytes supported the proliferation of murine CTLL cells and provided the basis for an IL-2 assay. Mitogen induced proliferative responses and IL-2 production of spleen cells but not lymph node cells from pre-patent and microfilaremic jirds were suppressed. Both B. pahangi Ag-induced proliferative responsiveness and IL-2 production of spleen cells from microfilaremic jirds were also suppressed relative to lymph node cells from the same animals or spleen cells from B. pahangi immunized or prepatent jirds. Depletion of histamine receptor-bearing cells restored the ability of spleen cells from microfilaremic jirds to produce significant levels of IL-2. In addition, in add-mixture experiments, spleen cells from microfilaremic jirds suppressed Ag-induced IL-2 production by cells from either B. pahangi- or KHL-immunized jirds. Exogenous IL-2 failed to reconstitute the suppressed Ag-induced proliferative response of spleen cells from microfilaremic jirds. This study demonstrates that the down-regulation of immune responses in B. pahangi infection is a cell-mediated event and is associated with an inability to produce IL-2.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Leiva</LastName><ForeName>L E</ForeName><Initials>LE</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Immunology and Parasitology, LSU Medical Center, New Orleans 70112.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lammie</LastName><ForeName>P J</ForeName><Initials>PJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>AI24459</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Immunol</MedlineTA><NlmUniqueID>2985117R</NlmUniqueID><ISSNLinking>0022-1767</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000947">Antigens, Helminth</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007376">Interleukin-2</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000947" MajorTopicYN="N">Antigens, Helminth</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002009" MajorTopicYN="N">Brugia</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004605" MajorTopicYN="N">Elephantiasis, Filarial</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005368" MajorTopicYN="N">Filariasis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005849" MajorTopicYN="N">Gerbillinae</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007376" MajorTopicYN="N">Interleukin-2</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007700" MajorTopicYN="N">Kinetics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008198" MajorTopicYN="N">Lymph Nodes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008213" MajorTopicYN="Y">Lymphocyte Activation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008842" MajorTopicYN="N">Microfilariae</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013154" MajorTopicYN="N">Spleen</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013601" MajorTopicYN="N">T-Lymphocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1989</Year><Month>2</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1989</Year><Month>2</Month><Day>15</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1989</Year><Month>2</Month><Day>15</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">2783709</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list></list><tree><noCountry><name sortKey="Lammie, P J" sort="Lammie, P J" uniqKey="Lammie P" first="P J" last="Lammie">P J Lammie</name><name sortKey="Leiva, L E" sort="Leiva, L E" uniqKey="Leiva L" first="L E" last="Leiva">L E Leiva</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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