IL-10 is pathogenic during the development of coxsackievirus B4-induced chronic pancreatitis.
IL-10 is pathogenic during the development of coxsackievirus B4-induced chronic pancreatitis.
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DOI：
10.1016/j.virol.2009.09.005
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发表时间：
2009-12-05
期刊：
影响因子：
3.7
通讯作者：
Ramsingh, Arlene I.
中科院分区：
文献类型：
--
作者：
Gu, Rui;Shampang, Anae;Reilly, Andrew;Fisher, Dusti;Glass, William;Ramsingh, Arlene I.
Using a mouse model of coxsackievirus B4 (CVB4-V)-induced chronic pancreatitis; we investigated whether cytokines are involved in the progression of acute disease to chronic inflammatory disease. We show that IL-10 contributed to the development of chronic pancreatitis since acute disease resolved when IL-10 was absent or when IL-10 signaling was disrupted. We explored the underlying mechanisms by which IL-10 affected disease progression, using a novel approach to assess immunological events occurring in situ. Multiple markers that define functional innate immune responses and functional T cell responses were monitored over the course of CVB4-V infection of wild-type and IL-10 knockout mice, using a multiplex transcriptional profiling approach. We show that high levels of IL-10 early during infection were associated with delayed innate and T cell responses. Furthermore, high IL-10 production correlated with altered kinetics of T regulatory responses indicating a disruption in the balance between effector and regulatory T cell responses.
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