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10.4110/in.2010.10.3.104

http://scihub22266oqcxt.onion/10.4110/in.2010.10.3.104
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C2902672!2902672!20631881
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suck abstract from ncbi


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pmid20631881      Immune+Netw 2010 ; 10 (3): 104-8
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  • Agonistic Anti-CD137 Monoclonal Antibody Treatment Induces CD11b+Gr-1+ Myeloid-derived Suppressor Cells #MMPMID20631881
  • Lee JM; Seo JH; Kim YJ; Kim YS; Ko HJ; Kang CY
  • Immune Netw 2010[Jun]; 10 (3): 104-8 PMID20631881show ga
  • CD137 (4-1BB/tnfrsf9) has been shown to co-stimulate T cells. However, agonistic anti-CD137 monoclonal antibody (mAb) treatment can suppress CD4+ T cells, ameliorating autoimmune diseases, whereas it induces activation of CD8+ T cells, resulting in diverse therapeutic activity in cancer, viral infection. To investigate the CD137-mediated T cell suppression mechanism, we examined whether anti-CD137 mAb treatment could affect CD11b+Gr-1+ myeloid-derived suppressor cells (MDSCs). Intriguingly, anti-CD137 mAb injection significantly increased CD11b+Gr-1+ cells, peaking at days 5 to 10 and continuing for at least 25 days. Furthermore, this cell population could suppress both CD8+ T cells and CD4+ T cells. Thus, this study demonstrated that, for the first time, anti-CD137 mAb treatment could induce CD11b+Gr-1+ MDSCs under normal conditions, suggesting a possible relationship between myeloid cell induction and CD137-mediated immune suppression.
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