Autoimmunity through cytokine-induced dendritic cell activation

Immunity. 2004 May;20(5):539-50. doi: 10.1016/s1074-7613(04)00108-6.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Autoimmunity / immunology*
  • Dendritic Cells / immunology*
  • Humans
  • Interferons / immunology*
  • Lymphocyte Activation / immunology
  • Models, Immunological*
  • Signal Transduction / immunology
  • Tumor Necrosis Factor-alpha / immunology*


  • Tumor Necrosis Factor-alpha
  • Interferons