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Type I interferon-mediated autoinflammation and autoimmunity

Stefanie Kretschmer¹, Min Ae Lee-Kirsch¹

¹Department of Pediatrics, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.

Current Opinion in Immunology

|November 13, 2017

Abstract:

The monogenic type I interferonopathies comprise a heterogenous group of disorders of the innate immune system associated with constitutive activation of antiviral type I interferon (IFN). Despite a remarkable phenotypic diversity, type I interferonopathies are commonly characterized by autoinflammation and varying degrees of autoimmunity or immunodeficiency. The elucidation of the underlying genetic causes has revealed novel cell-intrinsic mechanisms that protect the organism against inappropriate immune recognition of self nucleic acids by cytosolic sensors such as cGAS or MDA5 through metabolizing or processing of intracellular DNA or RNA. What emerges from these findings is a more integrated picture of the different modes by which unabated type I IFN causes autoinflammation or drives autoimmunity.

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