کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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6261977 | 1613273 | 2011 | 6 صفحه PDF | دانلود رایگان |

Experimental autoimmune neuritis (EAN) is a well-known animal model of human demyelinating polyneuropathies and is characterized by inflammation and demyelination in the peripheral nervous system. Tim-3 had been identified as a Th1-specific marker negatively regulating autoimmunity or inflammatory diseases. Here we have studied by immunohistochemistry the spatiotemporal accumulation of Tim-3+ cells in sciatic nerves of EAN rats, particularly focusing on its association with alternatively activated macrophages. Our results showed that time course of Tim-3+ cell accumulation correlated positively with disease progression of EAN; but distinct major cellular resources of Tim-3 were observed at different disease stages of EAN: during the early phase of EAN, the main cellular resource were T cells, but at the peak and during recovery phase of EAN, Tim-3 was mostly expressed on CD68+ macrophages or CD163+ cells. Further investigation suggested that accumulation of CD163+ cells, particularly their relative abundances to activated macrophages at different time points, were in accordance with the recovery from EAN. Therefore, Tim3+ cells might include a distinct macrophage population, which may be involved in anti-inflammatory effect and recovery from EAN.
⺠We studied by immunohistochemistry the spatiotemporal accumulation of Tim-3+ cells in sciatic nerves of experimental autoimmune neuritis (EAN) rats. ⺠Time course of Tim-3+ cell accumulation correlated positively with disease progression of EAN, but distinct major cellular resources of Tim-3 were observed at different disease stages. ⺠At the peak and during recovery phase of EAN, Tim-3 was mostly expressed on CD68+ macrophages or CD163+ cells. ⺠Tim3+ cells might include a distinct macrophage population, which may be involved in anti-inflammatory effect and recovery from EAN.
Journal: Brain Research Bulletin - Volume 86, Issues 3â4, 10 October 2011, Pages 229-234