2019
DOI: 10.1016/j.jaut.2018.12.004
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Crosstalk between tumor necrosis factor-alpha signaling and aryl hydrocarbon receptor signaling in nuclear factor –kappa B activation: A possible molecular mechanism underlying the reduced efficacy of TNF-inhibitors in rheumatoid arthritis by smoking

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Cited by 16 publications
(9 citation statements)
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“…Furthermore, cigarette smoking markedly induces inflammation and alters immune signaling pathways. Studies have shown that smoking can promote the body's inflammatory response by increasing the release of pro-inflammatory factors [42][43][44] . In addition, smoking leads to oxidative stress, which induces systemic inflammation.…”
Section: Discussionmentioning
confidence: 99%
“…Furthermore, cigarette smoking markedly induces inflammation and alters immune signaling pathways. Studies have shown that smoking can promote the body's inflammatory response by increasing the release of pro-inflammatory factors [42][43][44] . In addition, smoking leads to oxidative stress, which induces systemic inflammation.…”
Section: Discussionmentioning
confidence: 99%
“…for the exacerbation of RA in cigarette smokers (20)(21)(22). Indeed, activation of AHRs by the constituents of cigarette smoke can potentiate the induction of NFkB by Tumor Necrosis Factor-α (TNF-α), leading not only to increased inflammatory activity but also reducing the efficacy of anti-TNF-α medications and possibly explaining both the apparent resistance of some patients to these drugs but also the high rate of non-compliance or discontinuation (23). The mechanism of AHR in these cases is likely to involve changes in the number and activity of Th17 cells (21) consistent with the evidence noted above.…”
Section: Rheumatoid Arthritismentioning
confidence: 99%
“…However, it is still challenging to understand whether or how smoking work together with TNF blockade to orchestrate the psoriasis occurrence. In vitro , cigarette smoke chemical components could activate nuclear factor kappa-B activation and proinflammatory cytokine production, including IL-1β and IL-6 ( 50 ). The full blockade of TNF-α may impair the homeostasis of normal skin and cause an imbalance in cytokines and cells, which may be further exacerbated by the presence of smoking, and finally paradoxical adverse events occur ( 50 ).…”
Section: Discussionmentioning
confidence: 99%
“…In vitro , cigarette smoke chemical components could activate nuclear factor kappa-B activation and proinflammatory cytokine production, including IL-1β and IL-6 ( 50 ). The full blockade of TNF-α may impair the homeostasis of normal skin and cause an imbalance in cytokines and cells, which may be further exacerbated by the presence of smoking, and finally paradoxical adverse events occur ( 50 ). For paradoxical skin inflammation, the IFN-α pathway was considered to play a key role.…”
Section: Discussionmentioning
confidence: 99%