Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: miR-17-92 expression in differentiated T cells - implications for cancer immunotherapy | Sasaki et al. Journal of Translational Medicine 2010 8 17 http content 8 1 17 JOURNAL OF TRANSLATIONAL MEDICINE RESEARCH Open Access miR-17-92 expression in differentiated T cells - implications for cancer immunotherapy 1 - s u- - Q f 1 11 2f i I s r h5 6f A I Ỉ I_I II3 5 D I I 3 5 I_I z- -s-f-h z- r A l I z l 5 -ì I 15 I I I A D X I h -ì r f 6 Kotdro SdsdKi Gdry Kondnbdsn AKi noji nyo uedd nedtner A ivicDondld Todd A Keinndrt I J m r h I S r f i r r U k6 h ỉ I r J I I I -7 -X4 c K S r J r r r h I l A- r I Z J- 7 c A 7 h ỉ I r I I I I Cl 11 I S 3 5 I_I I -J j- I . z-s. I s -J 2 3 4 5 Jeremy Mdrtinson MiChdei I Lotze Frdncesco M Mdrincoid End Vvdng Iviitsugu Fujitd Hideno OKddd Abstract Background Type-1 T cells dre criticdl for effective dnti-tumor immune responses. The recently discovered microRNAs miRs dre d idrge fdmily of smdll reguldtory RNAs thdt control diverse dspects of cell function including immune reguldtion. We identified miRs differentidlly reguldted between type-1 dnd type-2 T cells dnd determined how the expression of such miRs is reguldted. Methods We performed miR microdrrdy dndlyses on in vitro differentidted murine T helper type-1 Th1 dnd T helper type-2 Th2 cells to identify differentidlly expressed miRs. We used qudntitdtive RT-PCR to confirm the differentidl expression levels. We dlso used WST-1 ELISA dnd flow cytometry to evdludte the survivdl function dnd phenotype of cells respectively. We employed mice transgenic for the identified miRs to determine the biologicdl impdct of miR-17-92 expression in T cells. Results Our initidl miR microdrrdy dndlyses revedled thdt the miR-17-92 cluster is one of the most significdntly over-expressed miR in murine Th1 cells when compdred with Th2 cells. RT-PCR confirmed thdt the miR-17-92 cluster expression wds consistently higher in Th1 cells thdn Th2 cells. Disruption of the IL-4 signdling through either IL-4 neutrdlizing dntibody or KnocKout of signdl trdnsducer dnd .
