Immune modulation by chondroitin sulfate and its degraded disaccharide product in the development of an experimental model of multiple sclerosis.
Immune modulation by chondroitin sulfate and its degraded disaccharide product in the development of an experimental model of multiple sclerosis.
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DOI：
10.1016/j.jneuroim.2010.04.002
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发表时间：
2010-06
影响因子：
3.3
通讯作者：
Nagarkatti M
中科院分区：
文献类型：
--
作者：
Zhou J;Nagarkatti P;Zhong Y;Nagarkatti M
mog诱导的EAE小鼠的临床症状在注射硫酸红血素A （CS-A）后显著加重，而给予降解产物CSPG-DS可显著抑制EAE的发展。此外，在EAE的临床症状出现后，给予CSPG-DS而不是CS-A，能够抑制疾病。进一步的研究表明CS-A上调STAT4的表达，从而诱导IFN-γ的产生和Th1 CD4 T细胞的分化。CS-A还上调STAT3和IL-23的表达，从而增加IL-17的产生。体内和体外CSPG-DS处理均可降低脾细胞TNFα的生成。体外和体内研究表明，CSPG-DS治疗EAE小鼠可明显阻断淋巴细胞的迁移，而CS-A治疗可增加脑内淋巴细胞的浸润。
Clinical symptoms in MOG-induced EAE mice significantly exacerbated following hondroitin sulfate A (CS-A) injection, whereas administration of a degraded product, CSPG-DS, caused dramatic inhibition of EAE development. Also, administration of CSPG-DS but not CS-A, after the onset of clinical symptoms of EAE, was able to suppress the disease. Further studies demonstrated that CS-A up-regulated STAT4 expression and thus, induced IFN-γ production and Th1 CD4 T cell differenttiation. CS-A also up-regulated STAT3 and IL-23 expression and thus increased IL-17 producing T cells. CSPG-DS treatment both in vivo and in vitro decreased TNFα production from splenocytes. In vitro and in vivo studies indicated that CSPG-DS treatment in EAE mice significantly blocked migration of lymphocytes, whereas CS-A treatment increased lymphocyte infiltration in the brain.
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影响因子：
4.8
作者：
Pure, Ellen;Assoian, Richard K.
通讯作者：
Assoian, Richard K.
DOI：
10.4049/jimmunol.0802325
发表时间：
2009-07-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Guan H;Nagarkatti PS;Nagarkatti M
通讯作者：
Nagarkatti M
影响因子：
7
作者：
Hochberg MC;Clegg DO
通讯作者：
Clegg DO
影响因子：
4.6
作者：
Baeurle, S. A.;Kiselev, M. G.;Nogovitsin, E. A.
通讯作者：
Nogovitsin, E. A.
影响因子：
158.5
作者：
Clegg, DO;Reda, DJ;Williams, HJ
通讯作者：
Williams, HJ