TNF-α–induced protein 3 (A20): The immunological rheostat

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Presentation transcript:

TNF-α–induced protein 3 (A20): The immunological rheostat Asher Maroof, PhD, Dhavalkumar D. Patel, MD, PhD Journal of Allergy and Clinical Immunology Volume 142, Issue 2, Pages 401-402 (August 2018) DOI: 10.1016/j.jaci.2018.05.020 Copyright © 2018 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 1 Schematic diagram depicting TNFR2-mediated inhibition of IL-17A through TNFAIP3 (A20). During early stages of T-cell receptor (TCR) signaling, nuclear factor of activated T cells (NFAT), along with other signaling cascades, is engaged. This leads to activation of the IL-2 promoter and consequently triggers expression of several proinflammatory mediators, such as IFN-γ, TNF-α, and IL-17A. Binding of TNFR2 by either soluble or membrane TNF-α promotes nuclear translocation of NF-κB and induction of proinflammatory and anti-inflammatory genes. A20 disrupts NF-κB signaling through sequential deubiquitination and ubiquitination of RIP1 but might also indirectly regulate IL-17A expression through the protein kinase C (PKC), p38, or phosphorylated signal transducer and activator of transcription 5 (pSTAT5) pathways. AP1, Activator protein 1; IL-2R, IL-2 receptor; RORγT, retinoic acid–related orphan receptor γT. Journal of Allergy and Clinical Immunology 2018 142, 401-402DOI: (10.1016/j.jaci.2018.05.020) Copyright © 2018 American Academy of Allergy, Asthma & Immunology Terms and Conditions