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International Immunology Advance Access originally published online on May 17, 2005
International Immunology 2005 17(6):721-728; doi:10.1093/intimm/dxh253
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© The Japanese Society for Immunology. 2005. All rights reserved. For permissions, please e-mail: journals.permissions@oupjournals.org

Featured Article of the Month

Co-infection with Trypanosoma brucei brucei prevents experimental autoimmune encephalomyelitis in DBA/1 mice through induction of suppressor APCs

Maja Wållberg and Robert A. Harris

Applied Immunology Unit, Centre for Molecular Medicine L8:04, Karolinska Institute, SE-17176 Stockholm, Sweden

Correspondence to: M. Wållberg; E-mail: maja.wallberg{at}cmm.ki.se

The immune system has co-evolved with the infectious agents that challenge it, and in response pathogens have developed different mechanisms to subvert host immunity. A wealth of evidence suggests that infections are important components in the development of a functional immune system, and understanding the modulation of the host immune system by pathogens may offer new therapeutic strategies in a non-infectious setting. We investigated how infection with the protozoan parasite Trypanosoma brucei brucei (Tbb) modulates the autoimmune response to recombinant myelin oligodendrocyte glycoprotein (rMOG) in DBA/1 mice. Mice harbouring a Tbb infection did not develop experimental autoimmune encephalomyelitis (EAE) induced by immunization with rMOG in CFA, an animal model for the human autoimmune disease multiple sclerosis. Additionally, mice infected with the parasite at the time of immunization or 1 week later developed less severe EAE than uninfected controls. Protected mice displayed a markedly diminished rMOG-specific proliferation and IFN{gamma} production in lymph node cells and had correspondingly low titres of serum anti-rMOG IgG. Antigen-presenting cells (APCs) from spleens of Tbb-infected mice presented rMOG less efficiently to rMOG-specific T cells in vitro than did splenic APCs from uninfected mice and could also inhibit antigen-specific proliferation in control in vitro cultures. This suppressive effect is at least in part due to increased release of IL-10. Transfer of splenic APCs from Tbb-infected mice into mice immunized with rMOG-CFA 7 days previously abrogated disease significantly. These findings indicate that infections can prevent autoimmunity and that APCs might be used as immunomodulants.

Keywords: autoimmunity, immunomodulation, parasite

Transmitting editor: A. Cooke


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