کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6020036 | 1580383 | 2016 | 5 صفحه PDF | دانلود رایگان |

- CCR4 antagonist Compound 22 ameliorated the clinical symptoms of EAE.
- Compound 22 inhibits Th1 and Th17 polarization.
- Compound 22 downregulated the T cell priming.
- CCR4 antagonism might be used to treat MS.
Chemokines and chemokine receptors play important roles in the immune response. We previously reported the pathogenic role of C-C chemokine receptor type 4 (CCR4) in experimental autoimmune encephalomyelitis (EAE). Here, we examined whether CCR4 antagonism modulates the disease course of EAE. Wild-type and CCR4-knockout mice were induced EAE and were administered Compound 22, an antagonist of CCR4. Compound 22 significantly ameliorated the severity of EAE in wild-type mice, but not in the CCR4-knockout mice. Compound 22 inhibited Th1 and Th17 polarization of antigen-induced T-cell responses. Therefore, CCR4 antagonists might be potential therapeutic agents for multiple sclerosis.
CCR4 antagonist, Compound 22 significantly ameliorated the severity of EAE in wild-type mice, but not in the CCR4-knockout mice. CCR4 antagonism might be potential therapeutic agents for multiple sclerosis.74
Journal: Journal of Neuroimmunology - Volume 291, 15 February 2016, Pages 54-58