Role of NLRs in the Regulation of Type I Interferon Signaling, Host Defense and Tolerance to Inflammation
Autor: | Thomas A. Kufer, Ioannis Kienes, Nora Mirza, Tanja Weidl, Mathias Chamaillard |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
Inflammation
Endogeny NLR Proteins Review Biology Adaptive Immunity Catalysis lcsh:Chemistry Inorganic Chemistry Immune system Interferon NOD-like receptors medicine Animals Humans Physical and Theoretical Chemistry Receptor lcsh:QH301-705.5 Molecular Biology innate immunity Spectroscopy Innate immune system Mechanism (biology) Organic Chemistry fungi immune regulation General Medicine antiviral Immunity Innate Computer Science Applications lcsh:Biology (General) lcsh:QD1-999 Virus Diseases Immunology Interferon Type I type I interferon Interferons medicine.symptom signaling Function (biology) medicine.drug Signal Transduction |
Zdroj: | International Journal of Molecular Sciences International Journal of Molecular Sciences, Vol 22, Iss 1301, p 1301 (2021) |
ISSN: | 1422-0067 |
Popis: | Type I interferon signaling contributes to the development of innate and adaptive immune responses to either viruses, fungi, or bacteria. However, amplitude and timing of the interferon response is of utmost importance for preventing an underwhelming outcome, or tissue damage. While several pathogens evolved strategies for disturbing the quality of interferon signaling, there is growing evidence that this pathway can be regulated by several members of the Nod-like receptor (NLR) family, although the precise mechanism for most of these remains elusive. NLRs consist of a family of about 20 proteins in mammals, which are capable of sensing microbial products as well as endogenous signals related to tissue injury. Here we provide an overview of our current understanding of the function of those NLRs in type I interferon responses with a focus on viral infections. We discuss how NLR-mediated type I interferon regulation can influence the development of auto-immunity and the immune response to infection. |
Databáze: | OpenAIRE |
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