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Updated: May 28, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Mitochondrial antiviral signaling protein (MAVS) monitors commensal bacteria and induces an immune response that
Xiao-Dong Li1, Yu-Hsin Chiu, Anisa S Ismail
1Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA.
Abstract:
RIG-I-like receptors (RLRs) activate host innate immune responses against virus infection through recruiting the mitochondrial adaptor protein MAVS (also known as IPS1, VISA, or CARDIF). Here we show that MAVS also plays a pivotal role in maintaining intestinal homeostasis. We found that MAVS knockout mice developed more severe mortality and morbidity than WT animals in an experimental model of colitis. Bone marrow transplantation experiments revealed that MAVS in cells of nonhematopoietic origin plays a dominant role in the protection against colitis. Importantly, RNA species derived from intestinal commensal bacteria activate the RIG-I-MAVS pathway to induce the production of multiple cytokines and antimicrobial peptides, including IFN-β and RegIIIγ. These results unveil a previously unexplored role of MAVS in monitoring intestinal commensal bacteria and maintaining tissue homeostasis.
Insights
Mitochondrial antiviral signaling protein (MAVS) is crucial for innate immunity and intestinal homeostasis. MAVS monitors gut bacteria, protecting against colitis by inducing cytokine and antimicrobial peptide production.
Area of Science:
- Immunology
- Gastroenterology
- Microbiology
Background:
- RIG-I-like receptors (RLRs) mediate antiviral innate immunity via the mitochondrial adaptor MAVS.
- MAVS is known for its role in antiviral responses.
- Its function in intestinal homeostasis remains largely unexplored.
Purpose of the Study:
- To investigate the role of MAVS in maintaining intestinal homeostasis.
- To determine MAVS's involvement in experimental colitis.
- To elucidate the mechanism by which MAVS interacts with gut microbiota.
Main Methods:
- Utilized MAVS knockout mice and wild-type (WT) mice in an experimental colitis model.
- Conducted bone marrow transplantation experiments to differentiate hematopoietic and non-hematopoietic MAVS roles.
- Analyzed cytokine and antimicrobial peptide production in response to bacterial RNA.
Main Results:
- MAVS knockout mice exhibited exacerbated mortality and morbidity during colitis compared to WT mice.
- MAVS in non-hematopoietic cells was found to be dominant in protecting against colitis.
- Intestinal commensal bacterial RNA activated the RIG-I-MAVS pathway, inducing IFN-β and RegIIIγ production.
Conclusions:
- MAVS plays a critical, previously unrecognized role in maintaining intestinal homeostasis.
- MAVS acts as a sensor for intestinal commensal bacteria, contributing to tissue protection.
- MAVS signaling is essential for regulating the gut immune response to microbial stimuli.
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