IndraLab
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IL9 activates inflammatory response. 123 / 124
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"Studies in mice showed that IL-9 is likely to modulate vaginal response to Candida in a time-dependent manner, initially favoring inflammation via NLRP3 activation and then tolerance to the fungus by stimulating IL-1Ra production, mast cell (MC) engagement and macrophage crawling [106,107]."
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"To examine the cytokine profile of CCR9 + Tm cells and determine whether it deviated toward the Th17 phenotype in SPMS, we sorted CCR9 + and CCR9 - Tm cells, stimulated them, and measured IL-4, IL-9, IL-10, IL-17A, GM-CSF, IFNgamma, and TNFalpha levels, which are known to modulate CNS inflammation."
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"It is not clear whether IL-9 itself promotes intestinal inflammation, whether IL-9 impacts the production of additional cytokines from Th1 or Th17 cells that can promote intestinal inflammation, or whether Th9 cells directly acquire the ability to secrete other inflammatory cytokines in this model."
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"Microbial control of basophil numbers may be of particular importance in light of a recent study demonstrating that IL-4 secreted from basophils controlled the function of lung natural helper cells and enhanced expression of CCL11, IL-5, IL-9 and IL-13 in a murine model of allergen induced airway inflammation XREF_BIBR."
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"For example, IL-9 is involved in protective immunity to Trichuris muris infections 31, promotes Treg activation and prevents excessive cartilage destruction and bone loss in arthritis 32, and promotes tissue repair by amplifying ILC2 function in helminth induced lung inflammation 33."
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"Important lymphokines are IL-2, IL-3, IL-4, IL-5, IL-6, IL-9, IL-10, IL-13, IL-14 and TNF-gamma.Prostaglandins are lipids that are made at sites of infection and tissue damage to produce inflammation and fever as part of the healing process.Acute-phase response is the term used for haematological, endocrinological and metabolic changes that follow (within hours or days) the onset of fever in response to infections or local damage to a tissue."
| PMC
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"Although livers from infected anti-IL-9 mAb treated mice appeared slightly shallower than the infected ones, no obvious difference in the size of a single egg granuloma in mice liver was detected between the two (P> 0.05), and these results differ from our findings in IL-17 blockage mice 7; which, indicated that the effect of IL-9 to induce inflammation in S. Japonicum infected mouse liver is limited, and may be related to the powerful function of IL-7 in recruiting inflammatory cells 27."
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"In our experiments we have tested the effects of IL-9-IL-10 producing T cells in vivo in the RAG-1-deficient mice, in the absence of T reg cells; under these experimental conditions, IL-9 produced by the IL-9-IL-10 producing T cells may act only on the effector T cells and potentiate their pro inflammatory functions and thus induce more severe and unusual tissue inflammation (e.g., peripheral neuritis), which is not normally observed with the transfer of effector T cells alone."
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"Although it has been shown that IL-9 may promote IL-13-mediated lung inflammation and mucus production, we found no difference in the frequency of lung infiltrated IL-13-expressing Th2 cells in IL-9-treated mice, suggesting that other cells may have mediated the inflammatory process."
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"Importantly, adoptive transfer of an enriched IL-9 (+) iNKT cell population leads to exacerbated allergic inflammation in the airways upon intranasal immunization with house dust mite, confirming the ability of IL-9-producing iNKT cells to mediate proinflammatory effects in vivo, as previously reported."
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"To examine whether the increased IL-9 production contributed to airway inflammation in SPC-TSLP mice, transgenic and littermate control mice were treated with 10 mug and mouse anti-IL-9, 50 mug and mouse anti-IL-4, or control antibodies intravenously twice a week for 4 weeks beginning at 6 weeks of age, when the transgenic mice began to develop airway inflammation."