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Overcoming Unresponsiveness in Experimental Autoimmune Encephalomyelitis EAE Resistant Mouse Strains by Adoptive Transfer and Antigenic Challenge
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Tolerogen-induced interferon-producing killer dendritic cells (IKDCs) protect against EAE.

Eduardo Huarte1, Agnieszka Rynda-Apple, Carol Riccardi

  • 1Department of Immunology and Infectious Diseases, Montana State University, 960 Technology Blvd., Bozeman, MT 59718, USA.

Journal of Autoimmunity
|October 25, 2011
PubMed
Summary

Interferon-producing killer dendritic cells (IKDCs) are crucial for resolving experimental autoimmune encephalomyelitis (EAE) after treatment with MOG-pσ1. These activated IKDCs eliminate harmful T cells and promote regulatory T cell recruitment, demonstrating their therapeutic potential in autoimmune diseases.

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Area of Science:

  • Immunology
  • Neuroimmunology
  • Autoimmunity

Background:

  • Natural killer (NK) cells and dendritic cells (DCs) bridge innate and adaptive immunity.
  • Interferon-producing killer DCs (IKDCs) represent a novel innate cell subset with characteristics of both DCs and NK cells.

Purpose of the Study:

  • To investigate the role of IKDCs in resolving experimental autoimmune encephalomyelitis (EAE) following treatment with a tolerizing agent, myelin oligodendrocyte glycoprotein (MOG) fused to reovirus protein σ1 (MOG-pσ1).

Main Methods:

  • Treatment of EAE with MOG-pσ1.
  • Recruitment analysis of activated IKDCs.
  • NK1.1 cell depletion experiments.
  • Assessment of IKDC cytotoxic activity against CD4(+) T cells and DCs.
  • Analysis of regulatory T cell recruitment to the central nervous system (CNS).
  • Evaluation of IKDC surface marker expression (HVEM, MHC class II).
  • Adoptive transfer of activated and unactivated IKDCs.
  • Assessment of IKDC antigen-presenting capacity.

Main Results:

  • MOG-pσ1 treatment induced IKDC activation and recruitment in EAE.
  • Disease resolution was impaired upon NK1.1 cell depletion.
  • Activated IKDCs exhibited cytotoxic activity against CD4(+) T cells and DCs, contributing to EAE remission.
  • IKDCs mediated MOG-specific regulatory T cell recruitment to the CNS.
  • MOG-pσ1-induced IKDCs expressed elevated HVEM, interacting with LIGHT(+) NK and T(eff) cells and BTLA(+) B cells.
  • Activated IKDCs were MHC class II(high) and conferred protection upon adoptive transfer.
  • Activated IKDCs displayed enhanced CD107a, PD-L1, and granzyme B expression and presented OVA.

Conclusions:

  • Activated IKDCs play an essential role in the resolution of MOG-pσ1-treated EAE.
  • HVEM(+) IKDCs demonstrate interventional potency for resolving autoimmune diseases.