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    <link>https://dspace.nii.res.in//https://dspace.nii.res.in/handle/123456789/143</link>
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    <pubDate>Thu, 02 Apr 2026 18:51:56 GMT</pubDate>
    <dc:date>2026-04-02T18:51:56Z</dc:date>
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      <title>Cutting Edge: ACVRL1 Signaling Augments CD8a+ Dendritic Cell Development</title>
      <link>https://dspace.nii.res.in//https://dspace.nii.res.in/handle/123456789/1349</link>
      <description>Title: Cutting Edge: ACVRL1 Signaling Augments CD8a+ Dendritic Cell Development
Authors: Tailor, Prafullakumar
Abstract: Dendritic cells (DCs) are a collection of different subtypes, each of which is characterized by specific surface markers, gene-expression patterns, and distinct functions. Members of the IFN regulatory factor family play critical roles in DC development and functions. Recently, Irf8 was shown to activate TGF-β signaling, which led to exacerbated neuroinflammation in the experimental autoimmune encephalomyelitis mouse model. We analyzed the effect of Irf8 on TGF-β/bone morphogenetic protein pathway-specific genes in DCs and identified Acvrl1, a type I TGF-β superfamily receptor, as a gene strongly induced by Irf8 expression. Among various DC subtypes, Acvrl1 is differentially expressed in CD8α(+) DCs. ACVRL1 signaling augmented Irf8-directed classical CD8α(+) DC development. Irf8 expression is essential for plasmacytoid DC and CD8α(+) DC development, and this study demonstrates that ACVRL1 signaling plays a pivotal role whereby it suppresses plasmacytoid DC development while enhancing that of CD8α(+) DCs, thus contributing to DC diversity development.</description>
      <pubDate>Fri, 01 Jan 2016 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://dspace.nii.res.in//https://dspace.nii.res.in/handle/123456789/1349</guid>
      <dc:date>2016-01-01T00:00:00Z</dc:date>
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