Expression patterns of CD56+ and CD16+ cells in renal transplant biopsies with acute rejection: Associations with microcirculation injuries and graft survival

    loading  Checking for direct PDF access through Ovid

Excerpt

Natural Killer cells (NK cells) attract interest of many researchers due their role in the immune system, especially in organ transplantation because they are able to exert immunological functions without previous antigen‐specific sensitization.1
The phenotype that define human NK cells is characterized by the absence of the T cell receptor complex and by expression of CD56, which can be also found on some T cells.2 CD16 can be found on NK cells and it binds the Fc portion of antibodies and mediates antibody‐dependent cellular cytotoxicity (ADCC) of target cells.3
In allograft rejection, NK cell infiltration often occurs before evidence of T cell infiltration and it is consistent with the role of these cells as early innate effector cells in immune response. There is a hypothesis that IFN‐γ produced by NK cells during interaction with allogeneic endothelial cells stimulates MHC class I and class II expression, making them more susceptible to attack by specific T cells and leading to higher recruitment of inflammatory cells to the graft.4
In solid organ transplants, endothelial cells are the first structures to have contact with the immune system of the recipient. Hence activation of the endothelium and the recruitment of inflammatory cells, including NK cells play a crucial role in transplant rejection mechanisms. An experimental study in vitro investigated interactions between human cells and microcirculation endothelial cells and found that endothelial activation with TNFα induced NK cytotoxicity suggesting a role for NK cells in allograft responses.6
The hypothesis of the study is that NK cell markers, CD56 and CD16, can be associated with microcirculation injury scores: peritubular capillaritis (ptc) and glomerulitis (g), and survival time in kidney allograft biopsies with acute rejection.

Related Topics

    loading  Loading Related Articles