2016
DOI: 10.1016/j.ejphar.2016.06.002
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Adalimumab ameliorates OVA-induced airway inflammation in mice: Role of CD4 + CD25 + FOXP3 + regulatory T-cells

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Cited by 11 publications
(8 citation statements)
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“…It was also found that CD4 + T cells were downregulated in the wild-type MLR, but the expression of CD4 + T cells in MLR with CNR2 knock-out did not change, suggesting a promoting role of the CNR2 on the proportion and activity of Treg cells. In their study of experimental autoimmune encephalomyelitis (EAE), Kong et al (47) found that the CNR2 selective agonist GP1a treatment of EAE mice inhibited the expression of RORγt, and IL-17 and Th17 differentiation, and enhanced the expression of FOXP3 and IL-10 and Treg differentiation (48,49), which suggested that CNR2 agonist activation may directly promote Treg differentiation, reduce Th17 differentiation, and affect the ratio and activity of Treg/Th17.…”
Section: Discussionmentioning
confidence: 99%
“…It was also found that CD4 + T cells were downregulated in the wild-type MLR, but the expression of CD4 + T cells in MLR with CNR2 knock-out did not change, suggesting a promoting role of the CNR2 on the proportion and activity of Treg cells. In their study of experimental autoimmune encephalomyelitis (EAE), Kong et al (47) found that the CNR2 selective agonist GP1a treatment of EAE mice inhibited the expression of RORγt, and IL-17 and Th17 differentiation, and enhanced the expression of FOXP3 and IL-10 and Treg differentiation (48,49), which suggested that CNR2 agonist activation may directly promote Treg differentiation, reduce Th17 differentiation, and affect the ratio and activity of Treg/Th17.…”
Section: Discussionmentioning
confidence: 99%
“…The pro-inflammatory cytokine IL-6 is one of the key biomarkers in both ARDS patients and animal models that can predict the morbidity and mortality of ARDS patients [30, 31]. IFN-γ, a Th1 associated pro-inflammatory cytokine, is known to be essential in airway inflammation and inducing the influx of neutrophils [32, 33]. As a major inducer of CXCL10, excessive production of IFN-γ and CXCL10 contributed to injury progression in ARDS [34].…”
Section: Discussionmentioning
confidence: 99%
“…However, the IFN-γ levels were enhanced by the LED treatment in the BAL of the LPS-injected mice. IFN-γ is an important Th1 associated pro-inflammatory cytokine that inhibits the leukocyte influx into the lungs and it is mainly secreted by lymphocytes 35 , 36 . Moreover, IFN-γ secretion secretion is also important during a resolution of inflammation and it is responsible for a limitation of inflammation in a tissue injury 37 .…”
Section: Discussionmentioning
confidence: 99%