BACKGROUND: Cancer testis antigens (CTAs) are a novel group of tumor associated 
antigens. Demethylating agent decitabine was reported to be able to up-regulate 
CTAs through its hypomethylation mechanism, thus enhance the immunogenicity of 
leukemia cells. However, few researches have ever focused on the questions that 
whether this immunostimulatory effect of decitabine could induce autologous CTA 
specific cytotoxic T lymphocytes (CTLs) in vivo, and if so, whether this effect 
contributes to disease control. In this study, we aimed to show that decitabine 
could induce specific autologous CTLs against some mouse CTAs in leukemia cells 
in vitro and in vivo.
METHODS: Several mouse CTAs were screened by RT-PCR. CTL specific to one of the 
CTAs named P1A was detected and sorted by P1A specific dimer by flow cytometry. 
The activity of specific CTLs was measured by real time RT-PCR.
RESULTS: We firstly screened expression of some CTAs in mouse leukemia cells 
before and after decitabine treatment and found that decitabine treatment did 
up-regulate expression of many CTAs. Then we measured the CTLs' activity 
specific to a mouse CTA P1A in vivo and showed that this activity increased 
after decitabine treatment. Finally, we sorted these in vivo induced P1A 
specific CTLs by flow cytometry and demonstrated their cytotoxicity against 
decitabine treated leukemia cells.
CONCLUSIONS: Our study showed the autologous immune response induced by 
decitabine in vivo. And more importantly, we firstly proved that this response 
may contribute to disease control. We believe that this immunostimulatory effect 
is another anti-cancer mechanism of decitabine, and this special effect would 
inspire new applications of decitabine in the field of leukemia treatment in the 
future.