Murine DN T-reg cells impart prolonged cardiac allograft survival. Mus musculus

Recent studies have demonstrated that both mouse and human alpha beta TCR(+)CD3(+)NK1.1(-)CD4(-)CD8- double-negative regulatory T (DN Treg) cells can suppress Ag-specific immune responses mediated by CD8+ and CD4+ T cells. To identify molecules involved in DN Treg cell function, we generated a panel of murine DN Treg clones, which specifically kill activated syngeneic CD8+ T cells. Through serial cultivation of DN Treg clones, mutant clones arose that lost regulatory capacity in vitro and in vivo. Although all allogeneic cardiac grafts in animals preinfused with tolerant CD4/CD8 negative 12 DN Treg clones survived over 100 days, allograft survival is unchanged following infusion of mutant clones (19.5 +/- 11.1 days) compared with untreated controls (22.8 +/- 10.5 days; p 50-fold higher, was also confirmed using FACS. These findings shed light on the mechanisms by which DN Treg cells down-regulate immune responses and prolong cardiac allograft survival. Type 2 experiment where functional DN T-reg cells (CN4 or TN12) were cy-3 labeled and co-hybridized with non-functional mutant cell lines (CN4.8 or CN12.8). Used 100 ug total-RNA each channel and no amplifaction. A transcript identification design type characterizes the length and position of transcripts and allows identification of all forms of transcripts in the genome. Keywords: transcript_identification_design Overall design: Using regression correlation