Logo image
Canonical wnt signaling in dendritic cells regulates Th1/Th17 responses and suppresses autoimmune neuroinflammation
Journal article   Peer reviewed

Canonical wnt signaling in dendritic cells regulates Th1/Th17 responses and suppresses autoimmune neuroinflammation

Amol Suryawanshi, Indumathi Manoharan, Yuan Hong, Daniel Swafford, Tanmay Majumdar, M Mark Taketo, Balaji Manicassamy, Pandelakis A Koni, Muthusamy Thangaraju, Zuoming Sun, …
The Journal of immunology (1950), Vol.194(7), pp.3295-3304
04/01/2015
DOI: 10.4049/jimmunol.1402691
PMCID: PMC4369436
PMID: 25710911

View Online

Abstract

Breakdown in immunological tolerance to self-Ags or uncontrolled inflammation results in autoimmune disorders. Dendritic cells (DCs) play an important role in regulating the balance between inflammatory and regulatory responses in the periphery. However, factors in the tissue microenvironment and the signaling networks critical for programming DCs to control chronic inflammation and promote tolerance are unknown. In this study, we show that wnt ligand-mediated activation of β-catenin signaling in DCs is critical for promoting tolerance and limiting neuroinflammation. DC-specific deletion of key upstream (lipoprotein receptor-related protein [LRP]5/6) or downstream (β-catenin) mediators of canonical wnt signaling in mice exacerbated experimental autoimmune encephalomyelitis pathology. Mechanistically, loss of LRP5/6-β-catenin-mediated signaling in DCs led to an increased Th1/Th17 cell differentiation but reduced regulatory T cell response. This was due to increased production of proinflammatory cytokines and decreased production of anti-inflammatory cytokines such as IL-10 and IL-27 by DCs lacking LRP5/6-β-catenin signaling. Consistent with these findings, pharmacological activation of canonical wnt/β-catenin signaling delayed experimental autoimmune encephalomyelitis onset and diminished CNS pathology. Thus, the activation of canonical wnt signaling in DCs limits effector T cell responses and represents a potential therapeutic approach to control autoimmune neuroinflammation.
T-Lymphocyte Subsets - immunology Wnt3A Protein - metabolism Low Density Lipoprotein Receptor-Related Protein-5 - genetics Encephalomyelitis, Autoimmune, Experimental - metabolism Dendritic Cells - immunology Encephalomyelitis, Autoimmune, Experimental - immunology Male Th1 Cells - immunology Th1 Cells - metabolism Low Density Lipoprotein Receptor-Related Protein-6 - genetics Th17 Cells - metabolism Gene Deletion Inflammation Mediators - metabolism Interleukin-10 - metabolism Th17 Cells - cytology Cell Differentiation Dendritic Cells - metabolism Encephalomyelitis, Autoimmune, Experimental - pathology Cytokines - metabolism Signal Transduction Mice, Transgenic Gene Knockout Techniques beta Catenin - metabolism Animals Wnt Signaling Pathway - drug effects T-Lymphocyte Subsets - metabolism Th17 Cells - immunology Mice Th1 Cells - cytology Transforming Growth Factor beta - metabolism

Details

Metrics

Logo image