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Haines, Brian B.,Ryu, Chun Jeih,Chang, Sandy,Protopopov, Alexei,Luch, Andreas,Kang, Yun Hee,Draganov, Dobrin D.,Fragoso, Maria F.,Paik, Sang Gi,Hong, Hyo Jeong,DePinho, Ronald A.,Chen, Jianzhu Cell Press 2006 CANCER CELL Vol.9 No.2
<P><B>Summary</B></P><P>Mice deficient in the DNA damage sensor P53 display normal T cell development but eventually succumb to thymic lymphomas. Here, we show that inactivation of the TCR β gene enhancer (Eβ) results in a block of T cell development at stages where recombination-activating genes (RAG) are expressed. Introduction of the Eβ mutation into <I>p53<SUP>−/−</SUP></I> mice dramatically accelerates the onset of lethal thymic lymphomas that harbor RAG-dependent aberrant rearrangements, chromosome 14 and 12 translocations, and amplification of the chromosomal region 9A1–A5.3. Phenotypic and genetic analyses suggest that lymphomas emerge through a normal thymocyte development pathway. These findings provide genetic evidence that block of lymphocyte development at stages with RAG endonuclease activity can provoke lymphomagenesis on a background with deficient DNA damage responses.</P>
Classical Flt3L-dependent dendritic cells control immunity to protein vaccine
Anandasabapathy, Niroshana,Feder, Rachel,Mollah, Shamim,Tse, Sze-Wah,Longhi, Maria Paula,Mehandru, Saurabh,Matos, Ines,Cheong, Cheolho,Ruane, Darren,Brane, Lucas,Teixeira, Angela,Dobrin, Joseph,Mizeni The Rockefeller University Press 2014 The Journal of experimental medicine Vol.211 No.9
<P>DCs are critical for initiating immunity. The current paradigm in vaccine biology is that DCs migrating from peripheral tissue and classical lymphoid-resident DCs (cDCs) cooperate in the draining LNs to initiate priming and proliferation of T cells. Here, we observe subcutaneous immunity is Fms-like tyrosine kinase 3 ligand (Flt3L) dependent. Flt3L is rapidly secreted after immunization; Flt3 deletion reduces T cell responses by 50%. Flt3L enhances global T cell and humoral immunity as well as both the numbers and antigen capture capacity of migratory DCs (migDCs) and LN-resident cDCs. Surprisingly, however, we find immunity is controlled by cDCs and actively tempered in vivo by migDCs. Deletion of Langerin<SUP>+</SUP> DC or blockade of DC migration improves immunity. Consistent with an immune-regulatory role, transcriptomic analyses reveals different skin migDC subsets in both mouse and human cluster together, and share immune-suppressing gene expression and regulatory pathways. These data reveal that protective immunity to protein vaccines is controlled by Flt3L-dependent, LN-resident cDCs.</P>