RIG-I-like receptors (RLRs), including RIG-I, MDA5, and LGP2, are critical for detecting viral RNA and initiating antiviral immune responses. These receptors recognize pathogen-associated molecular patterns (PAMPs) in the cytoplasm, triggering innate immunity and inflammation. RLRs interact with Toll-like receptors (TLRs) and other factors to modulate both innate and adaptive immune responses. RLR signaling is regulated at multiple levels, including autoregulation, ligand interactions, and post-translational modifications. Dysregulation of RLR signaling is linked to autoimmune diseases. RLRs detect viral RNA with 5' triphosphorylated ends, which are essential for signaling. RIG-I and MDA5 recognize different viral RNA structures, with RIG-I preferring shorter RNA fragments and MDA5 recognizing high molecular weight poly(I:C). LGP2 is thought to regulate RIG-I and MDA5 signaling. RLRs activate signaling pathways that lead to type I interferon (IFN) production and antiviral gene expression. RLR signaling is also involved in inflammatory responses and the regulation of adaptive immunity. RLRs interact with other PRRs, such as TLRs, to enhance immune responses. RLR signaling is regulated by ubiquitination, deubiquitination, and post-translational modifications, which control the timing and magnitude of immune responses. Genetic variations in RLRs may influence susceptibility to infections and autoimmune diseases. RLRs play a key role in both innate and adaptive immune responses, with their activity regulated by various mechanisms to ensure proper immune function and prevent excessive inflammation.RIG-I-like receptors (RLRs), including RIG-I, MDA5, and LGP2, are critical for detecting viral RNA and initiating antiviral immune responses. These receptors recognize pathogen-associated molecular patterns (PAMPs) in the cytoplasm, triggering innate immunity and inflammation. RLRs interact with Toll-like receptors (TLRs) and other factors to modulate both innate and adaptive immune responses. RLR signaling is regulated at multiple levels, including autoregulation, ligand interactions, and post-translational modifications. Dysregulation of RLR signaling is linked to autoimmune diseases. RLRs detect viral RNA with 5' triphosphorylated ends, which are essential for signaling. RIG-I and MDA5 recognize different viral RNA structures, with RIG-I preferring shorter RNA fragments and MDA5 recognizing high molecular weight poly(I:C). LGP2 is thought to regulate RIG-I and MDA5 signaling. RLRs activate signaling pathways that lead to type I interferon (IFN) production and antiviral gene expression. RLR signaling is also involved in inflammatory responses and the regulation of adaptive immunity. RLRs interact with other PRRs, such as TLRs, to enhance immune responses. RLR signaling is regulated by ubiquitination, deubiquitination, and post-translational modifications, which control the timing and magnitude of immune responses. Genetic variations in RLRs may influence susceptibility to infections and autoimmune diseases. RLRs play a key role in both innate and adaptive immune responses, with their activity regulated by various mechanisms to ensure proper immune function and prevent excessive inflammation.