Human life within a narrow range: The lethal ups and downs of type I interferons

Author:

Crow Yanick J.123ORCID,Casanova Jean-Laurent34567ORCID

Affiliation:

1. MRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.

2. Laboratory of Neurogenetics and Neuroinflammation, Imagine Institute, INSERM UMR 1163, Paris, France.

3. University Paris Cité, Paris, France.

4. St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, Rockefeller University, New York, NY, USA.

5. Howard Hughes Medical Institute, New York, NY, USA.

6. Department of Pediatrics, Necker Hospital for Sick Children, Paris, France.

7. Laboratory of Human Genetics of Infectious Diseases, Necker Branch, Imagine Institute, INSERM UMR 1163, Necker Hospital for Sick Children, Paris, France.

Abstract

The past 20 years have seen the definition of human monogenic disorders and their autoimmune phenocopies underlying either defective or enhanced type I interferon (IFN) activity. These disorders delineate the impact of type I IFNs in natural conditions and demonstrate that only a narrow window of type I IFN activity is beneficial. Insufficient type I IFN predisposes humans to life-threatening viral diseases (albeit unexpectedly few) with a central role in immunity to respiratory and cerebral viral infection. Excessive type I IFN, perhaps counterintuitively, appears to underlie a greater number of autoinflammatory and/or autoimmune conditions known as type I interferonopathies, whose study has revealed multiple molecular programs involved in the induction of type I IFN signaling. These observations suggest that the manipulation of type I IFN activity to within a physiological range may be clinically relevant for the prevention and treatment of viral and inflammatory diseases.

Publisher

American Association for the Advancement of Science (AAAS)

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