Wolbachia Lipoprotein Stimulates Innate and Adaptive Immunity through Toll-like Receptors 2 and 6 to Induce Disease Manifestations of Filariasis*
Identifieur interne : 006512 ( Main/Merge ); précédent : 006511; suivant : 006513Wolbachia Lipoprotein Stimulates Innate and Adaptive Immunity through Toll-like Receptors 2 and 6 to Induce Disease Manifestations of Filariasis*
Auteurs : Joseph D. Turner ; R. Stuart Langley ; Kelly L. Johnston ; Katrin Gentil ; Louise Ford ; Bo Wu [États-Unis] ; Maia Graham ; Faye Sharpley ; Barton Slatko [États-Unis] ; Eric Pearlman ; Mark J. TaylorSource :
- The Journal of Biological Chemistry [ 0021-9258 ] ; 2009.
Abstract
Url:
DOI: 10.1074/jbc.M901528200
PubMed: 19458089
PubMed Central: 2755959
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PMC:2755959Le document en format XML
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Lipoprotein Stimulates Innate and Adaptive Immunity through Toll-like Receptors 2 and 6 to Induce Disease Manifestations of Filariasis<xref ref-type="fn" rid="FN1">*</xref>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main"><italic>Wolbachia</italic>
Lipoprotein Stimulates Innate and Adaptive Immunity through Toll-like Receptors 2 and 6 to Induce Disease Manifestations of Filariasis<xref ref-type="fn" rid="FN1">*</xref>
<xref ref-type="fn" rid="FN2"><sup><inline-graphic xlink:href="sbox.jpg"></inline-graphic>
</sup>
</xref>
</title>
<author><name sortKey="Turner, Joseph D" sort="Turner, Joseph D" uniqKey="Turner J" first="Joseph D." last="Turner">Joseph D. Turner</name>
<affiliation><nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Langley, R Stuart" sort="Langley, R Stuart" uniqKey="Langley R" first="R. Stuart" last="Langley">R. Stuart Langley</name>
<affiliation><nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Johnston, Kelly L" sort="Johnston, Kelly L" uniqKey="Johnston K" first="Kelly L." last="Johnston">Kelly L. Johnston</name>
<affiliation><nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Gentil, Katrin" sort="Gentil, Katrin" uniqKey="Gentil K" first="Katrin" last="Gentil">Katrin Gentil</name>
<affiliation><nlm:aff id="aff2"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Ford, Louise" sort="Ford, Louise" uniqKey="Ford L" first="Louise" last="Ford">Louise Ford</name>
<affiliation><nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Wu, Bo" sort="Wu, Bo" uniqKey="Wu B" first="Bo" last="Wu">Bo Wu</name>
<affiliation wicri:level="2"><nlm:aff id="aff3">New England Biolabs, Ipswich, Massachusetts 01938</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Massachusetts</region>
</placeName>
<wicri:cityArea>New England Biolabs, Ipswich</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Graham, Maia" sort="Graham, Maia" uniqKey="Graham M" first="Maia" last="Graham">Maia Graham</name>
<affiliation><nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Sharpley, Faye" sort="Sharpley, Faye" uniqKey="Sharpley F" first="Faye" last="Sharpley">Faye Sharpley</name>
<affiliation><nlm:aff id="aff1"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Slatko, Barton" sort="Slatko, Barton" uniqKey="Slatko B" first="Barton" last="Slatko">Barton Slatko</name>
<affiliation wicri:level="2"><nlm:aff id="aff3">New England Biolabs, Ipswich, Massachusetts 01938</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Massachusetts</region>
</placeName>
<wicri:cityArea>New England Biolabs, Ipswich</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Pearlman, Eric" sort="Pearlman, Eric" uniqKey="Pearlman E" first="Eric" last="Pearlman">Eric Pearlman</name>
<affiliation><nlm:aff id="aff2"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Taylor, Mark J" sort="Taylor, Mark J" uniqKey="Taylor M" first="Mark J." last="Taylor">Mark J. Taylor</name>
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</affiliation>
</author>
</analytic>
<series><title level="j">The Journal of Biological Chemistry</title>
<idno type="ISSN">0021-9258</idno>
<idno type="eISSN">1083-351X</idno>
<imprint><date when="2009">2009</date>
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<front><div type="abstract" xml:lang="en"><p><italic>Wolbachia</italic>
endosymbiotic bacteria have been implicated in the inflammatory pathogenesis of filariasis. Inflammation induced by <italic>Brugia malayi</italic>
female worm extract (BMFE) is dependent on Toll-like receptors 2 and 6 (TLR2/6) with only a partial requirement for TLR1. Removal of <italic>Wolbachia</italic>
, lipids, or proteins eliminates all inflammatory activity. <italic>Wolbachia</italic>
bacteria contain the lipoprotein biosynthesis genes <italic>Ltg</italic>
and <italic>LspA</italic>
but not <italic>Lnt</italic>
, suggesting <italic>Wolbachia</italic>
proteins cannot be triacylated, accounting for recognition by TLR2/6. Lipoprotein databases revealed 3–11 potential lipoproteins from <italic>Wolbachia</italic>
. Peptidoglycan-associated lipoprotein (PAL) and Type IV secretion system-VirB6 were consistently predicted, and <italic>B. malayi Wolbachia</italic>
PAL (wBmPAL) was selected for functional characterization. Diacylated 20-mer peptides of wBmPAL (Diacyl <italic>Wolbachia</italic>
lipopeptide (Diacyl WoLP)) showed a near identical TLR2/6 and TLR2/1 usage compared with BMFE and bound directly to TLR2. Diacyl WoLP induced systemic tumor necrosis factor-α and neutrophil-mediated keratitis in mice. Diacyl WoLP activated monocytes induce up-regulation of gp38 on human lymphatic endothelial cells and induced dendritic cell maturation and activation. Dendritic cells primed with BMFE generated a non-polarized Th1/Th2 CD4<sup>+</sup>
T cell profile, whereas priming with <italic>Wolbachia</italic>
depleted extracts (following tetracycline treatment; BMFEtet) polarized to a Th2 profile that could be reversed by reconstitution with Diacyl WoLP. BMFE generated IgG1 and IgG2c antibody responses, whereas BMFEtet or inoculation of TLR2 or MyD88<sup>−/−</sup>
mice produced defective IgG2c responses. Thus, in addition to innate inflammatory activation, <italic>Wolbachia</italic>
lipoproteins drive interferon-γ-dependent CD4<sup>+</sup>
T cell polarization and antibody switching.</p>
</div>
</front>
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