A positive margin results in a significantly worse outcome for pT1-2, pN0-1, and I-II stage gastric cancer patients who undergo D2/D3 lymphadenectomy, but not for those in pT3-4, pN2-3, and III-IV stage.

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Summary CD83 is a surface marker expressed on matured dendritic cells (DCs). It plays a pivotal role in the mediation of DC/T cell interaction and induction of T‐cell activation. Previous studies have suggested that a soluble form of CD83 could suppress DC maturation and inhibit T‐cell activation and, as a result, it can prevent paralysis associated with experimental autoimmune encephalomyelitis. Here, we explored its potential effect on allograft rejection in a fully major histocompatibility complex‐mismatched murine skin transplantation model. A form of mouse soluble CD83 (CD83‐Ig) fused the extracellular domain of murine CD83 with human IgG1α Fc tail was purified from transfected COS‐7 cell. It was found that the treatment of recipient mice with CD83‐Ig significantly delayed allograft rejection. Especially, when T cells originated from recipients treated with CD83‐Ig re‐stimulated with donor‐specific splenocytes, they showed a significant reduced responding capability as compared with that of originated from control recipients. In line with these results, a reduction for serum IFN‐γ and IL‐2 and a decreased mRNA expression of IFN‐γ and IL‐2 in allograft infiltrated immune cells were also observed. Our results suggest that CD83‐Ig could be useful for the treatment of allograft rejection in combination with other therapeutic strategies.