Decreased IL-4 production in new onset type I insulin-dependent diabetes mellitus.

Decreased IL-4 production in new onset type I insulin-dependent diabetes mellitus.
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DOI:
10.4049/jimmunol.157.10.4690
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发表时间:
1996-11
影响因子:
4.4
通讯作者:
M. Berman;Christy Sandborg;Z. Wang;K. Imfeld;F. Zaldivar;V. Dadufalza;Bruce A. Buckingham
M. Berman;Christy Sandborg;Z. Wang;K. Imfeld;F. Zaldivar;V. Dadufalza;Bruce A. Buckingham
中科院分区:
医学2区
文献类型:
--
作者:
M. Berman;Christy Sandborg;Z. Wang;K. Imfeld;F. Zaldivar;V. Dadufalza;Bruce A. Buckingham

文献摘要

被引文献

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IL-4已显示在胰岛素依赖性(I型)糖尿病(IDDM)的啮齿动物模型中防止糖尿病发展。为了研究人IDDM中IL-4的产生,来自IDDM患者和对照的PBMC在体外用PHA、抗CD 3 mAb或PMA和离子载体刺激。在糖尿病发病时(p> 2年),IDDM患者PBMC或T细胞产生的IL-4严重受损,显示出广泛的IL-4应答,其平均IL-4应答低于对照组;然而,差异无统计学意义。使用竞争性逆转录PCR测量IL-4 mRNA水平。结果表明,在新发IDDM中mRNA水平大大降低。相比之下,IL-1的产生(ELISA法测定)和IFN-γ mRNA(逆转录PCR法测定)在IDDM中没有显著差异。结果表明,在胰岛素依赖型糖尿病发病时,炎症细胞因子与抗炎细胞因子的产生不平衡。如在IDDM发作时所见,IL-4产生不足可能通过允许胰岛中的炎症/自身免疫过程进展而在糖尿病的发展中发挥作用。
IL-4 has been shown to protect against diabetes development in rodent models of insulin-dependent (type I) diabetes mellitus (IDDM). To study IL-4 production in human IDDM, PBMC from IDDM patients and controls were stimulated in vitro with PHA, anti-CD3 mAb, or PMA and ionophore. IL-4 production by PBMC or T cells was strongly impaired in IDDM patients at diabetes onset (p 2 yr) showed a wide range of IL-4 responses and their mean IL-4 response was lower than the controls; however, the difference was not statistically significant. IL-4 mRNA levels were measured using competitive reverse transcription PCR. The results showed greatly reduced mRNA levels in new onset IDDM. In contrast, IL-1 production (measured by ELISA) and IFN-gamma mRNA (measured by reverse transcription PCR) were not significantly different in IDDM. The results suggest an imbalance of inflammatory vs anti-inflammatory cytokine production at the onset of IDDM. Deficient IL-4 production as seen at the onset of IDDM may play a role in the development of diabetes by allowing the inflammatory/autoimmune process in pancreatic islets to progress.