About this Research Topic
More than 60 years ago a soluble factor which “interferes” with influenza virus infection of mammalian cells was discovered and named “interferon”. It was later shown that this interferon (IFN) was actually composed of different proteins of the same family, which were found to play different roles in vertebrates. IFNs are very powerful cytokines that can activate more than 400 interferon-stimulated genes (ISGs), which ensure a complete antiviral response targeting all stages of the replicative cycles of different viruses. Type-I IFNs (IFN-I), which can be potentially produced by any cells, have strong antiproliferative and immunomodulatory activities, and are essential to control viral infection and spread. In most or all pathogenic virus infections, early production of type I IFN is required to limit initial viral replication before effective humoral or cellular adaptive immune mechanisms become operational.
However, sustained overproduction of IFN-I can be deleterious for the host. The negative impact of IFN-I is well illustrated by a class of disorders collectively termed type 1 interferonopathies composed of rare monogenic diseases and complex auto-inflammatory/auto immune diseases such as systemic lupus erythematosus (SLE).
Thus, since the last decade, there is a strong increasing scientific and clinical interest in elucidating the biology of IFN-I. Although our understanding of cellular and molecular functions of interferons has tremendously advanced recently, much remains to be learned and IFN-I remains an active and fascinating area of inquiry with promising clinical applications. All studies involving IFN-I, IFN signaling or IFN producing cells in normal or pathologic settings are welcome.
In this Research Topic, we welcome the submission of Original Research, Reviews, Mini Reviews, and Opinion articles focusing on the following subtopics:
1. New insights on type 1 interferonopathies
2. The roles of IFN-I in chronic viral infections
3. New therapies targeting IFN-I
4. Role of interferon producing cells in autoimmunity and inflammatory diseases.
Dr. Herbeuval is the co-founder of Ermium Therapeutics. The other Topic Editors declare no competing interests with regards to the Research Topic theme.
However, sustained overproduction of IFN-I can be deleterious for the host. The negative impact of IFN-I is well illustrated by a class of disorders collectively termed type 1 interferonopathies composed of rare monogenic diseases and complex auto-inflammatory/auto immune diseases such as systemic lupus erythematosus (SLE).
Thus, since the last decade, there is a strong increasing scientific and clinical interest in elucidating the biology of IFN-I. Although our understanding of cellular and molecular functions of interferons has tremendously advanced recently, much remains to be learned and IFN-I remains an active and fascinating area of inquiry with promising clinical applications. All studies involving IFN-I, IFN signaling or IFN producing cells in normal or pathologic settings are welcome.
In this Research Topic, we welcome the submission of Original Research, Reviews, Mini Reviews, and Opinion articles focusing on the following subtopics:
1. New insights on type 1 interferonopathies
2. The roles of IFN-I in chronic viral infections
3. New therapies targeting IFN-I
4. Role of interferon producing cells in autoimmunity and inflammatory diseases.
Dr. Herbeuval is the co-founder of Ermium Therapeutics. The other Topic Editors declare no competing interests with regards to the Research Topic theme.
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
