Interleukin 1 (IL-1)- and IL-23-Mediated Expansion of Filarial Antigen-Specific Th17 and Th22 Cells in Filarial Lymphedema
Identifieur interne : 001A80 ( Pmc/Checkpoint ); précédent : 001A79; suivant : 001A81Interleukin 1 (IL-1)- and IL-23-Mediated Expansion of Filarial Antigen-Specific Th17 and Th22 Cells in Filarial Lymphedema
Auteurs : R. Anuradha [Inde] ; P. Jovvian George [Inde] ; V. Chandrasekaran [Inde] ; P. Paul Kumaran [Inde] ; Thomas B. Nutman [États-Unis] ; Subash Babu [Inde, États-Unis]Source :
- Clinical and Vaccine Immunology : CVI [ 1556-6811 ] ; 2014.
Abstract
Lymphatic filarial disease is known to be associated with elevated Th1 responses and normal or diminished Th2 responses to parasite-specific antigens. The roles of Th17 cells and the recently described Th22 cells have not been examined in detail in either filarial infection itself or in filarial disease (e.g., lymphedema and elephantiasis). To explore the roles of Th17 and Th22 cells and their subsets, we examined the frequencies of these cells in individuals with filarial lymphedema (chronic pathology [CP]), in clinically asymptomatic infected (INF) individuals, and in uninfected (UN) individuals
Url:
DOI: 10.1128/CVI.00257-14
PubMed: 24807054
PubMed Central: 4097448
Affiliations:
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<front><div type="abstract" xml:lang="en"><p>Lymphatic filarial disease is known to be associated with elevated Th1 responses and normal or diminished Th2 responses to parasite-specific antigens. The roles of Th17 cells and the recently described Th22 cells have not been examined in detail in either filarial infection itself or in filarial disease (e.g., lymphedema and elephantiasis). To explore the roles of Th17 and Th22 cells and their subsets, we examined the frequencies of these cells in individuals with filarial lymphedema (chronic pathology [CP]), in clinically asymptomatic infected (INF) individuals, and in uninfected (UN) individuals <italic>ex vivo</italic>
and in response to parasite and nonparasite antigens. Those with disease (CP) had significantly expanded frequencies of Th17 and Th22 cells, compared with either INF or UN individuals, at baseline (<italic>ex vivo</italic>
) and in response to parasite antigens. This antigen-driven expansion of Th17 and Th22 cells was dependent on interleukin 1 (IL-1), IL-23, and, to lesser extent, transforming growth factor β (TGF-β), as blockade of any of these cytokines resulted in significantly diminished frequencies of Th17 and Th22 cells. Our findings, therefore, suggest that filarial parasite-driven expansion of Th17 and Th22 cells is associated with the pathogenesis of filarial infections and disease.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Clin Vaccine Immunol</journal-id>
<journal-id journal-id-type="iso-abbrev">Clin. Vaccine Immunol</journal-id>
<journal-id journal-id-type="hwp">cdli</journal-id>
<journal-id journal-id-type="pmc">cvi</journal-id>
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<issn pub-type="epub">1556-679X</issn>
<publisher><publisher-name>American Society for Microbiology</publisher-name>
<publisher-loc>1752 N St., N.W., Washington, DC</publisher-loc>
</publisher>
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<article-meta><article-id pub-id-type="pmid">24807054</article-id>
<article-id pub-id-type="pmc">4097448</article-id>
<article-id pub-id-type="publisher-id">00257-14</article-id>
<article-id pub-id-type="doi">10.1128/CVI.00257-14</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Clinical Immunology</subject>
</subj-group>
</article-categories>
<title-group><article-title>Interleukin 1 (IL-1)- and IL-23-Mediated Expansion of Filarial Antigen-Specific Th17 and Th22 Cells in Filarial Lymphedema</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Anuradha</surname>
<given-names>R.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>George</surname>
<given-names>P. Jovvian</given-names>
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<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Chandrasekaran</surname>
<given-names>V.</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>b</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kumaran</surname>
<given-names>P. Paul</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>b</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Nutman</surname>
<given-names>Thomas B.</given-names>
</name>
<xref ref-type="aff" rid="aff3"><sup>c</sup>
</xref>
</contrib>
<contrib contrib-type="author" corresp="yes"><name><surname>Babu</surname>
<given-names>Subash</given-names>
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<xref ref-type="aff" rid="aff1"><sup>a</sup>
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<xref ref-type="aff" rid="aff3"><sup>c</sup>
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<aff id="aff1"><label>a</label>
National Institutes of Health, International Center for Excellence in Research, Chennai, India</aff>
<aff id="aff2"><label>b</label>
National Institute for Research in Tuberculosis, Chennai, India</aff>
<aff id="aff3"><label>c</label>
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA</aff>
</contrib-group>
<contrib-group><contrib contrib-type="editor"><name><surname>Wilkins</surname>
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</contrib>
</contrib-group>
<author-notes><corresp id="cor1">Address correspondence to Subash Babu, <email>sbabu@mail.nih.gov</email>
.</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>7</month>
<year>2014</year>
</pub-date>
<volume>21</volume>
<issue>7</issue>
<fpage>960</fpage>
<lpage>965</lpage>
<history><date date-type="received"><day>25</day>
<month>4</month>
<year>2014</year>
</date>
<date date-type="accepted"><day>1</day>
<month>5</month>
<year>2014</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2014, American Society for Microbiology. All Rights Reserved.</copyright-statement>
<copyright-year>2014</copyright-year>
<copyright-holder>American Society for Microbiology</copyright-holder>
</permissions>
<self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zcd00714000960.pdf"></self-uri>
<abstract><p>Lymphatic filarial disease is known to be associated with elevated Th1 responses and normal or diminished Th2 responses to parasite-specific antigens. The roles of Th17 cells and the recently described Th22 cells have not been examined in detail in either filarial infection itself or in filarial disease (e.g., lymphedema and elephantiasis). To explore the roles of Th17 and Th22 cells and their subsets, we examined the frequencies of these cells in individuals with filarial lymphedema (chronic pathology [CP]), in clinically asymptomatic infected (INF) individuals, and in uninfected (UN) individuals <italic>ex vivo</italic>
and in response to parasite and nonparasite antigens. Those with disease (CP) had significantly expanded frequencies of Th17 and Th22 cells, compared with either INF or UN individuals, at baseline (<italic>ex vivo</italic>
) and in response to parasite antigens. This antigen-driven expansion of Th17 and Th22 cells was dependent on interleukin 1 (IL-1), IL-23, and, to lesser extent, transforming growth factor β (TGF-β), as blockade of any of these cytokines resulted in significantly diminished frequencies of Th17 and Th22 cells. Our findings, therefore, suggest that filarial parasite-driven expansion of Th17 and Th22 cells is associated with the pathogenesis of filarial infections and disease.</p>
</abstract>
</article-meta>
</front>
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