Toll-like receptors and IFN-alpha: partners in autoimmunity.
Many autoimmune diseases are thought to be precipitated by viral infections. In this issue of the JCI, Lang et al. demonstrate that, in a mouse model of autoimmune hepatitis, viral infections not only trigger expansion of self-reactive T cells but also activate antigen-presenting cells through TLR stimulation (see the related article beginning on page 2456). Activated cells then secrete IFN-alpha and TNF-alpha, which trigger tissue release of chemokines that attract self-reactive CD8+ T cells, ultimately leading to liver damage.
Colonna
Marco
M
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri 63110, USA. mcolonna@pathology.wustl.edu
D001327:Autoimmune Diseases / Q000276:immunology; D015551:Autoimmunity; D001402:B-Lymphocytes / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology; D006801:Humans; D016898:Interferon-alpha / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology; D051196:Toll-Like Receptor 3 / Q000276:immunology*; D051193:Toll-Like Receptors / Q000276:immunology*
D016207:Cytokines; D016898:Interferon-alpha; C495344:TLR3 protein, human; D051196:Toll-Like Receptor 3; D051193:Toll-Like Receptors