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Experimental autoimmune encephalomyelitis induction in naive mice by dendritic cells presenting a self‐peptide
Author(s) -
Weir Catherine R,
Nicolson Kirsty,
Bäckström B Thomas
Publication year - 2002
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1046/j.1440-1711.2002.01056.x
Subject(s) - experimental autoimmune encephalomyelitis , myelin oligodendrocyte glycoprotein , immunology , autoimmunity , antigen , antigen presenting cell , t cell , encephalomyelitis , bone marrow , biology , multiple sclerosis , medicine , immune system
Self‐reactive T cells escape deletion in the thymus and are found in the peripheral repertoire. Because bone‐marrow‐derived dendritic cells (BM‐DC) are potent activators of antigen‐specific T cells, these cells could theoretically activate self‐reactive T cells leading to autoimmunity. We investigated whether BM‐DC could induce the autoimmune disease experimental autoimmune encephalomyelitis (EAE). Our results show that transfer of BM‐DC presenting a self‐peptide from the myelin oligodendrocyte glycoprotein (MOG 35–55 ) into naive mice induced EAE 7–14 days later. MOG 35–55 ‐specific T cells of the Th1 phenotype were present in the lymph nodes and spleens of mice that received live peptide‐pulsed BM‐DC. Heat‐killed or formaldehyde‐fixed BM‐DC presenting MOG 35–55 could induce neither clinical signs of EAE nor a measurable T‐cell response in vitro . These data show that live BM‐DC presenting a self‐antigen can induce the organ‐specific autoimmune disorder EAE in a non‐transgenic system. Therefore, this new EAE model could be used as a more clinically relevant model for the human disease multiple sclerosis. These findings could also have implications for the use of DC immunotherapy in a clinical setting.