ArticlePloS one2014
A20 is critical for the induction of Pam3CSK4-tolerance in monocytic THP-1 cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- TLR2 and TLR4 bridge physiological and pathological inflammation in the reproductive system.Communications biology · 2025Review
- Interactions between toll-like receptors signaling pathway and gut microbiota in host homeostasis.Immunity, inflammation and disease · 2024Review
- Lipopolysaccharide Tolerance in Human Primary Monocytes and Polarized Macrophages.International journal of molecular sciences · 2023Article
- Article
- A data-driven computational model enables integrative and mechanistic characterization of dynamic macrophage polarization.iScience · 2021Article
- Tumour Necrosis Factor Alpha-induced Protein 3 Negatively Regulates Cutibacterium acnes-induced Innate Immune Events in Epidermal Keratinocytes.Acta dermato-venereologica · 2021Article
- IL-1α and IL-1β promote NOD2-induced immune responses by enhancing MAPK signaling.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Transcriptome Profiling of Bovine Macrophages Infected byFrontiers in immunology · 2019Article
- A20 upregulation during treated HIV disease is associated with intestinal epithelial cell recovery and function.PLoS pathogens · 2018Article
- SMAD4 is Involved in the Development of Endotoxin Tolerance in Microglia.Cellular and molecular neurobiology · 2016Article
- A20 regulates IL-1-induced tolerant production of CXC chemokines in human mesangial cells via inhibition of MAPK signaling.Scientific reports · 2015Article
- Technical advance: live-imaging analysis of human dendritic cell migrating behavior under the influence of immune-stimulating reagents in an organotypic model of lung.Journal of leukocyte biology · 2014Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A20 functions to terminate Toll-like receptor (TLR)-induced immune response, and play important roles in the induction of lipopolysacchride (LPS)-tolerance. However, the molecular mechanism for Pam3CSK4-tolerance is uncertain. Here we report that TLR1/2 ligand Pam3CSK4 induced tolerance in monocytic THP-1 cells. The pre-treatment of THP-1 cells with Pam3CSK4 down-regulated the induction of pro-inflammatory cytokines induced by Pam3CSK4 re-stimulation. Pam3CSK4 pre-treatment also down-regulated the signaling transduction of JNK, p38 and NF-κB induced by Pam3CSK4 re-stimulation. The activation of TLR1/2 induced a rapid and robust up-regulation of A20, suggesting that A20 may contribute to the induction of Pam3CSK4-tolerance. This hypothesis was proved by the observation that the over-expression of A20 by gene transfer down-regulated Pam3CSK4-induced inflammatory responses, and the down-regulation of A20 by RNA interference inhibited the induction of tolerance. Moreover, LPS induced a significant up-regulation of A20, which contributed to the induction of cross-tolerance between LPS and Pam3CSK4. A20 was also induced by the treatment of THP-1 cells with TNF-α and IL-1β. The pre-treatment with TNF-α and IL-1β partly down-regulated Pam3CSK4-induced activation of MAPKs. Furthermore, pharmacologic inhibition of GSK3 signaling down-regulated Pam3CSK4-induced A20 expression, up-regulated Pam3CSK4-induced inflammatory responses, and partly reversed Pam3CSK4 pre-treatment-induced tolerance, suggesting that GSK3 is involved in TLR1/2-induced tolerance by up-regulation of A20 expression. Taken together, these results indicated that A20 is a critical regulator for TLR1/2-induced pro-inflammatory responses.
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