Physiological functions of RIG-I-like receptors

Yoneyama, Mitsutoshi; Kato, Hiroki; Fujita, Takashi

doi:10.1016/j.immuni.2024.03.003

Cited by 10 publications

(1 citation statement)

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“…Thus, stimulus or PRR type determines the downstream immunoregulatory functioning of the PGAM5, including glycolysis support or MAVS-dependent type 1 IFN release. Details of RLR signaling in the infection and immunity have been discussed elsewhere [ 224 , 239 – 242 ]. The following sections discuss RLR signaling-induced IR and the impact of IR induced by other PRRs on RLR signaling.…”

Section: Rlr Signaling Pathway In Irmentioning

confidence: 99%

Pattern-Recognition Receptors and Immunometabolic Reprogramming: What We Know and What to Explore

Kumar,

Stewart IV

2024

J Innate Immun

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Background: Evolutionarily, immune response is a complex mechanism that protects the host from internal and external threats. Pattern-recognition receptors (PRRs) recognize MAMPs, PAMPs, and DAMPs to initiate a protective pro-inflammatory immune response. PRRs are expressed on the cell membranes by TLR1, 2, 4, and 6 and in the cytosolic organelles by TLR3, 7, 8, and 9, NLRs, ALRs, and cGLRs. We know their downstream signaling pathways controlling immunoregulatory and pro-inflammatory immune response. However, the impact of PRRs on metabolic control of immune cells to control their pro- and anti-inflammatory activity has not been discussed extensively. Summary: Immune cell metabolism or immunometabolism critically determines immune cells’ pro-inflammatory phenotype and function. The current article discusses immunometabolic reprogramming (IR) upon activation of different PRRs, such as TLRs, NLRs, cGLRs, and RLRs. The duration and type of PRR activated, species studied, and location of immune cells to specific organ are critical factors to determine the IR-induced immune response. Key Message: The work herein describes IR upon TLR, NLR, cGLR, and RLR activation. Understanding IR upon activating different PRRs is critical for designing better immune cell-specific immunotherapeutics and immunomodulators targeting inflammation and inflammatory diseases.

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Section: Rlr Signaling Pathway In Irmentioning

confidence: 99%

Pattern-Recognition Receptors and Immunometabolic Reprogramming: What We Know and What to Explore

Kumar,

Stewart IV

2024

J Innate Immun

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Innate Immune Response and Epigenetic Regulation: A Closely Intertwined Tale in Inflammation

Jawale,

Khandibharad,

Singh

2024

Advanced Biology

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Maintenance of delicate homeostasis is very important in various diseases because it ensures appropriate immune surveillance against pathogens and prevents excessive inflammation. In a disturbed homeostatic condition, hyperactivation of immune cells takes place and interplay between these cells triggers a plethora of signaling pathways, releasing various pro‐inflammatory cytokines such as Tumor necrosis factor alpha (TNFα), Interferon‐gamma (IFNƴ), Interleukin‐6 (IL‐6), and Interleukin‐1 beta (IL‐1β), which marks cytokine storm formation. To be precise, dysregulated balance can impede or increase susceptibility to various pathogens. Pathogens have the ability to hijack the host immune system by interfering with the host's chromatin architecture for their survival and replication in the host cell. Cytokines, particularly IL‐6, Interleukin‐17 (IL‐17), and Interleukin‐23 (IL‐23), play a key role in orchestrating innate immune responses and shaping adaptive immunity. Understanding the interplay between immune response and the role of epigenetic modification to maintain immune homeostasis and the structural aspects of IL‐6, IL‐17, and IL‐23 can be illuminating for a novel therapeutic regimen to treat various infectious diseases. In this review, the light is shed on how the orchestration of epigenetic regulation facilitates immune homeostasis.

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