title: Autoimmunity through cytokine-induced dendritic cell activation.
abstract: We propose a model where autoimmunity can be viewed as a dynamic system driven by opposite vectors IFN-alpha/beta and TNF. These cytokines drive differentiation of distinct types of DCs, TNF-DCs, or IFN-DCs, which present different antigens leading to distinct autoimmune responses. When balanced, both cytokines synergize in protective immunity. When one of the cytokines prevails, autoimmunity occurs, Type I interferons (IFN-alpha/beta) playing a major role in systemic lupus erythematosus (SLE) and TNF playing a major role in rheumatoid arthritis. This model complements the Type 1/Type 2 paradigm. Therefore, immunity can be viewed as a dynamic system driven by two sets of opposite vectors: IFN-alpha/beta/TNF and IFN-gamma/IL-4.
authors.affiliation: Baylor Institute for Immunology Research, 3434 Live Oak, Dallas, TX 75204 USA.
authors.forename: Jacques
authors.initials: J
authors.lastname: Banchereau
authors.forename: Virginia
authors.initials: V
authors.lastname: Pascual
authors.forename: A Karolina
authors.initials: AK
authors.lastname: Palucka
mesh_terms: D000818:Animals; D015551:Autoimmunity / Q000276:immunology*; D003713:Dendritic Cells / Q000276:immunology*; D006801:Humans; D007372:Interferons / Q000276:immunology*; D008213:Lymphocyte Activation / Q000276:immunology; D018448:Models, Immunological; D015398:Signal Transduction / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology*
chemical_list: D014409:Tumor Necrosis Factor-alpha; D007372:Interferons