Abstract:
BACKGROUND/AIMS:The expression of transcription factor Zbtb1 is essential for the maintenance and development of various blood cells in the hematopoietic system. In the current study, we found that the total number of thymocytes in PLZF deficient mice was reduced compared with thymocytes in wild-type mice, and the number of early T-cell progenitors decreased. However, the decrease of thymocytes in PLZF deficient mice was not cell intrinsic. This study adds new information regarding the regulation of the PLZF gene in the development and self-renewal of T cells. METHODS:The thymus was isolated from newborn mice, and the two lobes of each thymus were physically separated. Each host received a thymus, two lobes, each placed at one end of the kidney, as described in the literature. Tail vein blood was periodically collected from some of the recipients and analyzed for the presence of peripheral blood T cells. RESULTS:In PLZF-EGFP reporter mice and neonatal thymus transplantation to the kidney, we found that PLZF was highly expressed in DN1 (Lineage-CD44+CD25-) cells of thymic grafts of Rag2/γc-/- recipient mice. We found that the proportion of PLZF wild-type and mutant-derived cells in the thymocytes of recipient mice after bone marrow transplantation is approximately equal to the competitive bone marrow chimeric mouse model, and all mice contain a normal thymus. CONCLUSION:The development of T cells suggests that the effect of the PLZF gene on T cell differentiation and development is not cell intrinsic. However, in the neonatal mouse thymic transplant model in the Rag2/γc-/- recipient mouse, deletion of the PLZF gene results in a significant decrease in the proportion of DN1 cells from the donor in the thymic graft.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Du JL,Cao X,Liu HY,Zeng Y,Yang XC,Wan XM,Chang FF,Zhao TY,Jia XY,Wang HZ,Liu J,Cai KZ,Ma ZRdoi
10.1016/j.bbrc.2019.02.156subject
Has Abstractpub_date
2019-04-16 00:00:00pages
935-940issue
4eissn
0006-291Xissn
1090-2104pii
S0006-291X(19)30371-7journal_volume
511pub_type
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