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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
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Mitochondria in innate immune signaling
Balaji Banoth1, Suzanne L Cassel1
1Women's Guild Lung Institute, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
Summary
Mitochondria regulate innate immunity by releasing damage signals and controlling immune signaling pathways. Their metabolic state also fine-tunes immune cell responses to various stimuli.
Area of Science:
- Cell Biology
- Immunology
- Metabolism
Background:
- Mitochondria are vital for cellular energy production.
- Emerging evidence highlights their crucial role in innate immunity.
- Mitochondrial dysfunction can trigger immune responses.
Purpose of the Study:
- To elucidate the multifaceted roles of mitochondria in regulating innate immune responses.
- To explore how mitochondrial components and metabolites influence immune signaling.
- To understand the impact of mitochondrial metabolic status on immune cell function.
Main Methods:
- Review of current literature on mitochondrial function and innate immunity.
- Analysis of signaling pathways involving mitochondria in immune cells.
- Investigation of mitochondrial damage-associated molecular patterns (DAMPs).
Main Results:
- Mitochondrial components act as danger signals recognized by innate immune receptors.
- Mitochondria regulate key steps in innate immune signaling cascades.
- Mitochondrial metabolites and metabolic state profoundly modulate immune cell responses.
Conclusions:
- Mitochondria are central regulators of innate immunity, beyond their metabolic functions.
- Mitochondrial integrity and metabolic status are critical determinants of immune outcomes.
- Targeting mitochondrial pathways offers potential therapeutic strategies for immune modulation.
Keywords:
ASC, Apoptosis Associated Speck like protein containing CARDASK1, apoptosis signal-regulating kinase 1ATP, adenosine tri-phosphateCAPS, cryopyrin associated periodic syndromesCARD, caspase activation and recruitment domainCL, cardiolipinCLR, C-type lectin receptorCREB, cAMP response element binding proteinCgas, cyclic GMP-AMP synthaseDAMP, damage associated molecular patternESCIT, evolutionarily conserved signaling intermediate in the toll pathwayETC, electron transport chainFPR, formyl peptide receptorHIF, hypoxia-inducible factorHMGB1, high mobility group box protein 1IFN, interferonIL, interleukinIRF, interferon regulatory factorJNK, cJUN NH2-terminal kinaseLPS, lipopolysaccharideLRR, leucine rich repeatMAPK, mitogen-activated protein kinaseMARCH5, membrane-associated ring finger (C3HC4) 5MAVS, mitochondrial antiviral signalingMAVS, mitochondrial antiviral signaling proteinMFN1/2, mitofusinMOMP, mitochondrial outer membrane permeabilizationMPT, mitochondrial permeability transitionMyD88, myeloid differentiation primary response 88NADH, nicotinamide adenine dinucleotideNBD, nucleotide binding domainNFκB, Nuclear factor κ BNLR, NOD like receptorNOD, nucleotide-binding oligomerization domainNRF2, nuclear factor erythroid 2-related factor 2PAMP, pathogen associated molecular patternPPAR, peroxisome proliferator-accelerated receptorPRRs, pathogen recognition receptorsRIG-I, retinoic acid inducible gene IRLR, retinoic acid inducible gene like receptorROS, reactive oxygen speciesSTING, stimulator of interferon geneTAK1, transforming growth factor-β-activated kinase 1TANK, TRAF family member-associated NFκB activatorTBK1, TANK Binding Kinase 1TCA, Tri-carboxylic acidTFAM, mitochondrial transcription factor ATLR, Toll Like ReceptorTRAF6, tumor necrosis factor receptor-associated factor 6TRIF, TIR-domain-containing adapter-inducing interferon βTUFM, Tu translation elongation factor.fMet, N-formylated methioninemROS, mitochondrial ROSmtDNA, mitochondrial DNAn-fp, n-formyl peptides
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