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HLA-Ig Based Artificial Antigen Presenting Cells for Efficient ex vivo Expansion of Human CTL
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Cutting Edge: ACVRL1 Signaling Augments CD8α+ Dendritic Cell Development

Rohit Verma1, Hemant Jaiswal1, Kuldeep Singh Chauhan1

  • 1Laboratory of Innate Immunity, National Institute of Immunology, New Delhi, Delhi 110067, India.

Journal of Immunology (Baltimore, Md. : 1950)
|July 17, 2016
PubMed

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.

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