[HTML][HTML] Autoimmunity through cytokine-induced dendritic cell activation

J Banchereau, V Pascual, AK Palucka - Immunity, 2004 - cell.com
J Banchereau, V Pascual, AK Palucka
Immunity, 2004cell.com
We propose a model where autoimmunity can be viewed as a dynamic system driven by
opposite vectors IFN-α/β 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-α/β) playing a major role
in systemic lupus erythematosus (SLE) and TNF playing a major role in rheumatoid arthritis …
Abstract
We propose a model where autoimmunity can be viewed as a dynamic system driven by opposite vectors IFN-α/β 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-α/β) 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-α/β/TNF and IFN-γ/IL-4.
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