MHC class II–restricted antigen presentation by plasmacytoid dendritic cells inhibits T cell–mediated autoimmunity

Author:

Irla Magali1,Küpfer Natalia1,Suter Tobias2,Lissilaa Rami3,Benkhoucha Mahdia1,Skupsky Jonathan4,Lalive Patrice H.15,Fontana Adriano2,Reith Walter1,Hugues Stéphanie1

Affiliation:

1. Department of Pathology, University of Geneva Medical School, 1211 Geneva, Switzerland

2. Section of Clinical Immunology, University Hospital, 8044 Zürich, Switzerland

3. NovImmune SA, 1228 Plan-Les-Ouates, Geneva, Switzerland

4. Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, MD 21201

5. Division of Neurology and Laboratory Medicine Service, University Hospital of Geneva, 1211 Geneva, Switzerland

Abstract

Although plasmacytoid dendritic cells (pDCs) express major histocompatibility complex class II (MHCII) molecules, and can capture, process, and present antigens (Ags), direct demonstrations that they function as professional Ag-presenting cells (APCs) in vivo during ongoing immune responses remain lacking. We demonstrate that mice exhibiting a selective abrogation of MHCII expression by pDCs develop exacerbated experimental autoimmune encephalomyelitis (EAE) as a consequence of enhanced priming of encephalitogenic CD4+ T cell responses in secondary lymphoid tissues. After EAE induction, pDCs are recruited to lymph nodes and establish MHCII-dependent myelin-Ag–specific contacts with CD4+ T cells. These interactions promote the selective expansion of myelin-Ag–specific natural regulatory T cells that dampen the autoimmune T cell response. pDCs thus function as APCs during the course of EAE and confer a natural protection against autoimmune disease development that is mediated directly by their ability to present of Ags to CD4+ T cells in vivo.

Publisher

Rockefeller University Press

Subject

Immunology,Immunology and Allergy

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