Retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) are key sensors of viral dsRNA in the cytoplasm of both immune and non-immune cells. The engagement of RLRs drives the transcriptional induction of type 1 IFN (IFNa/ß) production and antiviral gene expression that establishes an antiviral immune response. RLRs include the three DExD/H box RNA helicases LGP2 (Laboratory of Genetics and Physiology 2), DHX58, RIG-I, and MDA5 (melanoma differentiation-associated protein 5, or IFIH1, or AGS7).
It has been recently understood that genetic material from the viruses and the host can activate RLRs, which leads to the induction of an effective antiviral immune response but also pathologies including malignancies and autoimmune diseases if uncontrolled. Therefore, RLRs are under tight control by regulatory mechanisms including non-coding RNAs and post-transcriptional modifications, though more research is required to understand their distinctive roles and functionality.
In this Research Topic, we aim to provide an update on the function and regulation of RLRs in antiviral immune responses, as well as in pathologies such as cancer, autoimmune disease, and immunopathologies. Relatedly, we will aim to review the regulatory mechanisms controlling the pathogenic and host-mediated activation of RLRs. We will also welcome the submission of studies utilizing our knowledge of RLR biology to develop novel therapeutics for use as antivirals, as well as in treating related cancers, autoimmune diseases, and immunopathologies.
In this Research Topic, we welcome the submission of Original Research, Review, and Mini Review articles focusing on RIG-I-Like Receptor-Mediated Innate Immune Responses. We welcome submissions covering, but not limited to, the following sub-topics:
• Updates on the antiviral sensing mechanisms of RLRs
• Updates on the antiviral immune responses initiated by activation of RLRs
• Host-derived triggers initiating activation of RLRs
• RLRs in the pathogenesis of cancer, autoimmune diseases, and immunopathologies
• Regulation of RLRs including by non-coding RNAs and Post-Transcriptional Modification
• Therapeutic potential of RLRs
Retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) are key sensors of viral dsRNA in the cytoplasm of both immune and non-immune cells. The engagement of RLRs drives the transcriptional induction of type 1 IFN (IFNa/ß) production and antiviral gene expression that establishes an antiviral immune response. RLRs include the three DExD/H box RNA helicases LGP2 (Laboratory of Genetics and Physiology 2), DHX58, RIG-I, and MDA5 (melanoma differentiation-associated protein 5, or IFIH1, or AGS7).
It has been recently understood that genetic material from the viruses and the host can activate RLRs, which leads to the induction of an effective antiviral immune response but also pathologies including malignancies and autoimmune diseases if uncontrolled. Therefore, RLRs are under tight control by regulatory mechanisms including non-coding RNAs and post-transcriptional modifications, though more research is required to understand their distinctive roles and functionality.
In this Research Topic, we aim to provide an update on the function and regulation of RLRs in antiviral immune responses, as well as in pathologies such as cancer, autoimmune disease, and immunopathologies. Relatedly, we will aim to review the regulatory mechanisms controlling the pathogenic and host-mediated activation of RLRs. We will also welcome the submission of studies utilizing our knowledge of RLR biology to develop novel therapeutics for use as antivirals, as well as in treating related cancers, autoimmune diseases, and immunopathologies.
In this Research Topic, we welcome the submission of Original Research, Review, and Mini Review articles focusing on RIG-I-Like Receptor-Mediated Innate Immune Responses. We welcome submissions covering, but not limited to, the following sub-topics:
• Updates on the antiviral sensing mechanisms of RLRs
• Updates on the antiviral immune responses initiated by activation of RLRs
• Host-derived triggers initiating activation of RLRs
• RLRs in the pathogenesis of cancer, autoimmune diseases, and immunopathologies
• Regulation of RLRs including by non-coding RNAs and Post-Transcriptional Modification
• Therapeutic potential of RLRs