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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-CD137mAb 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.
An autologous hybridoma antibody (4F1) against the phosphorylcholine-binding MOPC167 BALB/c myeloma protein was raised by cell fusion with splenocytes immunized with MOPC167. The anti-idiotype specificity of 4F1 was determined using a panel of different myeloma immunoglobulin. The data shows that 4F1 is an anti-idiotype antibody specific for MOPC167. The fine specificity of 4F1 was analyzed by inhibition of 4F1 binding to MOPC167 using free heavy and light chains of antibodies. The results indicate that 4F1 binding to MOPC167 is inhibited by the heavy chain of MOPC167, suggesting that an idiotope is located on the heavy chain. The nucleotide sequences of variable region genes of 4F1 were determined. Sequence analysis indicates that the genes encoding the variable region of 4F1 are completely unrelated to the genes encoding the MOPC167. However, genetic origin analysis shows that the V_H genes of the three sequenced anti-idiotype antibodies in the PC system belong to the same V_H gene family.