INT60694
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Our aim was to investigate the role of adrenoceptors in the modulation of in vivo interleukin-10 (IL-10) production in lipopolysaccharide (LPS)-treated mice. | |||||||||||||||
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Our aim was to investigate the role of adrenoceptors in the modulation of in vivo interleukin-10 (IL-10) production in lipopolysaccharide (LPS)-treated mice. | |||||||||||||||
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Our results provide the first in vivo evidence that, in addition to beta-adrenoceptors; alpha-adrenoceptors play also a very important role in the regulation of IL-10 production under endotoxaemic conditions. | |||||||||||||||
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Our results confirmed the involvement of beta-adrenoceptors since the beta-agonist isoproterenol significantly increased the IL-10 production in response to LPS stimulation, whereas the beta-antagonists propranolol decreased it. | |||||||||||||||
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Opposite role of alpha2- and beta-adrenoceptors in the modulation of interleukin-10 production in endotoxaemic mice. | |||||||||||||||
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Therefore, the absence of IL-10 expression accelerates the kinetics of lesion expansion, the onset of pain behaviors, and the peripheral immune response to spinal cord injury. | |||||||||||||||
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However, the role of endogenous production of IL-10 has not been considered. | |||||||||||||||
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OBJECTIVE: To investigate the expression of interleukin-10 (IL-10) in adenomyosis. | |||||||||||||||
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Expression of interleukin-10 in patients with adenomyosis. | |||||||||||||||
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OBJECTIVE: To investigate the expression of interleukin-10 (IL-10) in adenomyosis. | |||||||||||||||
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MAIN OUTCOME MEASURE(S): Microscopic evaluation to assess the presence and localization of IL-10 throughout the menstrual cycle in both eutopic endometrial and adenomyotic tissues of women with adenomyosis and compare it with IL-10 expression in the normal endometrium. | |||||||||||||||
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Some IL-10 was produced but only from non-T cells. | |||||||||||||||
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Epstein-Barr virus (EBV) takes advantage of the immunomodulatory effects of IL-10 by expressing a viral homolog of IL-10 during infections [6]. | |||||||||||||||
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We found that CD4+ T cells produce a significant amount of IL-10 and may be a major cellular source of IL-10 in vivo during WNV infection. | |||||||||||||||
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Our data also indicate that macrophages produce IL-10 when exposed to WNV ex vivo (Figure 1 A and B), which is consistent with in vivo results showing that CD11b+ macrophages produce low levels of IL-10. | |||||||||||||||
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Our data also indicate that macrophages produce IL-10 when exposed to WNV ex vivo (Figure 1 A and B), which is consistent with in vivo results showing that CD11b+ macrophages produce low levels of IL-10. | |||||||||||||||
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However, excessive IL-10 production suppresses host immune responses and can inadvertently facilitate the ability of intracellular pathogens to escape host innate immune defenses. | |||||||||||||||
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In addition, recent studies showed that lymphocytic choriomeningitis virus (LCMV) clone 13 elicits high levels of IL-10 production from the infected host, thereby resulting in exhaustion of virus-specific T cells and viral persistence [7][9]. | |||||||||||||||
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Intrapancreatic IL-10 gene expression was assessed by semiquantitative RT-PCR, and intrapancreatic collagen content was assessed by picrosirius staining. | |||||||||||||||
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Finally, two independent reports have demonstrated that blockade of the IL-10 receptor during chronic lymphocytic choriomeningitis virus infection led to clearance of the infection with enhanced IL-10 production by dendritic cells [63],[64]. | |||||||||||||||
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