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Decreased production of human leukocyte antigen G molecules in sinonasal polyposis.

机译:鼻窦息肉病中人类白细胞抗原G分子的产量减少。

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BACKGROUND: Sinonasal polyposis (SNP) is a chronic inflammatory pathology of nasal and paranasal cavities. Human leukocyte antigen (HLA) G molecules are nonclassic class I antigens with anti-inflammatory and tolerogenic properties. As most theories consider polyps to be the manifestation of chronic inflammation, there could be a possible implication of HLA-G molecules in SNP. The purpose of this study was to investigate the possible correlation between SNP and the production of soluble HLA-G (sHLA-G) by peripheral blood mononuclear cells (PBMCs). METHODS: The study involved 22 SNP patients (11 with no evidence of disease [NED] after surgery and 11 with relapse [RE]) and 20 healthy subjects. The presence of sHLA-G in PBMC lipopolysaccharide (LPS)-stimulated culture supernatants was analyzed. The levels of interleukin (IL) 10, one of the main up-regulators of sHLA-G production, were determined. Exogenous IL-10 was added to the SNP PBMC cultures to reconstitute the impairment in sHLA-G production. RESULTS: Increased IL-10 levels in LPS-activated PBMC culture supernatants were found in NED patients in comparison with healthy subjects (p = 0.0184). No sHLA-G production was observed in either of the patient subgroup supernatants (p < 0.0001). The addition of exogenous IL-10 showed the reconstitution of sHLA-G production in NED and in a lower amount in RE patients. CONCLUSION: The results show a defect in sHLA-G production in SNP patients mainly related to the IL-10/HLA-G pathway. Given the anti-inflammatory functions of HLA-G molecules, this impairment could increase the susceptibility to the disease. The different sHLA-G production after exogenous IL-10 addition between NED and RE SNP could represent a marker of disease severity.
机译:背景:鼻息肉病(SNP)是鼻腔和鼻腔的慢性炎症病理。人白细胞抗原(HLA)G分子是具有抗炎和致耐受性的非经典I类抗原。由于大多数理论认为息肉是慢性炎症的表现,因此SNP中可能含有HLA-G分子。这项研究的目的是调查外周血单核细胞(PBMC)的SNP与可溶性HLA-G(sHLA-G)的产生之间的可能关系。方法:该研究涉及22例SNP患者(11例术后无疾病[NED]和11例复发[RE])和20例健康受试者。分析了PBMC脂多糖(LPS)刺激的培养上清液中sHLA-G的存在。确定了sHLA-G产生的主要上调剂之一白介素(IL)10的水平。将外源IL-10添加到SNP PBMC培养物中以重建sHLA-G产生中的损伤。结果:与健康受试者相比,在NED患者中发现LPS激活的PBMC培养上清液中IL-10水平升高(p = 0.0184)。在任一患者亚组上清液中均未观察到sHLA-G产生(p <0.0001)。外源性IL-10的添加显示NED中sHLA-G产生的重构,而在RE患者中更低。结论:结果显示SNP患者sHLA-G产生缺陷主要与IL-10 / HLA-G途径有关。考虑到HLA-G分子的抗炎功能,这种损害可能会增加对该疾病的敏感性。 NED和RE SNP之间加入外源IL-10后产生的不同sHLA-G可能代表疾病严重程度。

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