Type I interferon (IFN-I) is a pleiotropic cytokine and belongs to the interferon family. Innate immune responses, which are activated by the recognition of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors(PRRs), are typically generated by IFN-I, which includes IFNa and IFNß. IFN-I is secreted and binds to a heterodimeric complex IFNAR consisting of IFNAR1 and IFNAR2, followed by phosphorylation and activation of signal transducers and activators of transcription 1 (STAT1) and STAT2, leading to the expression of IFN stimulated genes (ISG). Damage-associated molecular patterns can also trigger IFN-I production, which, as well as regulation of IFN-I signaling, might result in disastrous inflammation. IFN-I is not only involved in the protection against viral infections but also other immunologically relevant scenarios, including bacterial infections, cancer, and autoimmune and neurodegenerative diseases. It has been demonstrated that blocking the production of IFN-I and ISG through genetic deletion or pharmacological suppression of IFN-I signaling molecules can halt the progression of various disorders. Thus, targeting IFN-I-related signaling pathways will shed light on promising therapeutic applications in IFN-I-related diseases.
To advance research on the control of IFN-I induction and its subsequent biological effects under physiological and pathological situations, this section seeks to provide a platform for a review of our most recent knowledge of IFN-I production and function. Additionally, this subject will offer more thorough research of IFN-I responses in human disorders and may aid in the development of therapeutics.
This section seeks to attract submissions on the regulation of IFN-I production, as well as the therapeutic development based on the IFN-I. More specifically, the topics to be covered include:
1) The molecular mechanism underlying the regulation of IFN-I production.
2) The molecular mechanism underlying the regulation of IFN-I signaling.
3) Regulation of IFN-I pathways in viral diseases, autoimmunity, neurodegenerative disease, and cancer.
4) Molecular mechanism of IFN-I pathways in controlling inflammation.
5) Development of new technology to study IFN-I pathways.
6) Therapeutic development on targeting the IFN-I pathways.
7) Clinical applications of recombinant IFN-I.
Type I interferon (IFN-I) is a pleiotropic cytokine and belongs to the interferon family. Innate immune responses, which are activated by the recognition of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors(PRRs), are typically generated by IFN-I, which includes IFNa and IFNß. IFN-I is secreted and binds to a heterodimeric complex IFNAR consisting of IFNAR1 and IFNAR2, followed by phosphorylation and activation of signal transducers and activators of transcription 1 (STAT1) and STAT2, leading to the expression of IFN stimulated genes (ISG). Damage-associated molecular patterns can also trigger IFN-I production, which, as well as regulation of IFN-I signaling, might result in disastrous inflammation. IFN-I is not only involved in the protection against viral infections but also other immunologically relevant scenarios, including bacterial infections, cancer, and autoimmune and neurodegenerative diseases. It has been demonstrated that blocking the production of IFN-I and ISG through genetic deletion or pharmacological suppression of IFN-I signaling molecules can halt the progression of various disorders. Thus, targeting IFN-I-related signaling pathways will shed light on promising therapeutic applications in IFN-I-related diseases.
To advance research on the control of IFN-I induction and its subsequent biological effects under physiological and pathological situations, this section seeks to provide a platform for a review of our most recent knowledge of IFN-I production and function. Additionally, this subject will offer more thorough research of IFN-I responses in human disorders and may aid in the development of therapeutics.
This section seeks to attract submissions on the regulation of IFN-I production, as well as the therapeutic development based on the IFN-I. More specifically, the topics to be covered include:
1) The molecular mechanism underlying the regulation of IFN-I production.
2) The molecular mechanism underlying the regulation of IFN-I signaling.
3) Regulation of IFN-I pathways in viral diseases, autoimmunity, neurodegenerative disease, and cancer.
4) Molecular mechanism of IFN-I pathways in controlling inflammation.
5) Development of new technology to study IFN-I pathways.
6) Therapeutic development on targeting the IFN-I pathways.
7) Clinical applications of recombinant IFN-I.
