Open AccessA limited course of soluble CD83 delays acute cellular rejection of MHC‐mismatched mouse skin allografts
Author(s) -
Xu JunFa,
Huang BaoJun,
Yin Hui,
Xiong Ping,
Feng Wei,
Xu Yong,
Fang Min,
Zheng Fang,
Wang CongYi,
Gong FeiLi
Publication year - 2007
Publication title -
transplant international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.998
H-Index - 82
eISSN - 1432-2277
pISSN - 0934-0874
DOI - 10.1111/j.1432-2277.2006.00426.x
Subject(s) - immunology , major histocompatibility complex , medicine , transplantation , dendritic cell , immune system , transplant rejection , experimental autoimmune encephalomyelitis , t cell
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 IgG1 α 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.