Bidirectional modulation between infiltrating CD3(+) T-lymphocytes and astrocytes in the spinal cord drives the development of allodynia in monoarthritic rats.
Bidirectional modulation between infiltrating CD3(+) T-lymphocytes and astrocytes in the spinal cord drives the development of allodynia in monoarthritic rats.
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脊髓中浸润性 CD3 T 淋巴细胞和星形胶质细胞之间的双向调节驱动单关节炎大鼠异常性疼痛的发生
DOI：
10.1038/s41598-017-18357-z
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发表时间：
2018-01-08
影响因子：
4.6
通讯作者：
Xu H
中科院分区：
文献类型：
--
作者：
Zhou YL;Zhou SZ;Li HL;Hu ML;Li H;Guo QH;Deng XM;Zhang YQ;Xu H
Increasing evidence suggests that T cells and glia participate in the process of neuropathic pain. However, little is known about the involvement of T cells or the interaction between glia and T cells at the molecular level. Here we investigated the phenotype of T cell infiltration into the spinal cord in inflammatory pain and explored potential crosstalk between glia and T cells. The establishment of monoarthritis produced T cell infiltration and astrocyte activation, exhibiting similar kinetics in the spinal cord. T-cell-deficient (Rag1−/−) mice significantly attenuated MA-induced mechanical allodynia and GFAP upregulation. Double immunofluorescence staining showed that CD3 mainly colocalized with interferon-gamma (IFN-γ). Western blot and flow cytometry showed that multiple intrathecal administrations of astrocytic inhibitor fluorocitrate decreased IFN-γ-production without decreasing T cell number in the spinal cord. Spinal IFN-γ blockade reduced MA-induced mechanical allodynia and astroglial activation. In contrast, treatment with rIFN-γ directly elicited persistent mechanical allodynia and upregulation of GFAP and pJNK1/2 in naïve rats. Furthermore, rIFN-γ upregulated the phosphorylation of NF-κB p65 in cultured astrocytes vitro and spinal dorsal horn vivo. The results suggest that Th1 cells and astrocytes maintain inflammatory pain and imply that there may be a positive feedback loop between these cells via IFN-γ.
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影响因子：
25
作者：
Sorge RE;Mapplebeck JC;Rosen S;Beggs S;Taves S;Alexander JK;Martin LJ;Austin JS;Sotocinal SG;Chen D;Yang M;Shi XQ;Huang H;Pillon NJ;Bilan PJ;Tu Y;Klip A;Ji RR;Zhang J;Salter MW;Mogil JS
通讯作者：
Mogil JS
影响因子：
7.4
作者：
Gao YJ;Xu ZZ;Liu YC;Wen YR;Decosterd I;Ji RR
通讯作者：
Ji RR
影响因子：
2.5
作者：
Gao, Yong-Jing;Ji, Ru-Rong
通讯作者：
Ji, Ru-Rong
影响因子：
5.3
作者：
McKelvey, Rebecca;Berta, Temugin;Fitzgerald, Maria
通讯作者：
Fitzgerald, Maria
影响因子：
3.3
作者：
Sweitzer, SM;White, KA;DeLeo, JA
通讯作者：
DeLeo, JA