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Regulation of thymocyte homeostasis by Fliz1
Author(s) -
Hwang Eun Sook,
Ho ICheng
Publication year - 2002
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2002.01455.x
Subject(s) - thymocyte , biology , zinc finger , homeostasis , microbiology and biotechnology , apoptosis , haematopoiesis , progenitor cell , transgene , progenitor , gene , stem cell , t cell , immunology , transcription factor , genetics , immune system
Summary Fliz1 (fetal liver zinc finger protein 1) is a novel zinc finger protein preferentially expressed in fetal liver hematopoietic progenitors and in several adult organs, including the thymus. To investigate the in vivo function of Fliz1 in regulating the development of T cell lineage, we generated and studied transgenic mice overexpressing human Fliz1 in a T‐cell specific and inducible manner. We found that overexpression of human Fliz1 in adult animals resulted in a substantial decrease in total number of thymocytes due to enhanced apoptosis, whereas maturation of thymocytes remained undisturbed. The Fliz1‐induced apoptosis is dependent on the N‐terminus of Fliz1, which contains an acidic and a serine‐rich domains, and might be due to augmented expression of bad , a pro‐apoptotic gene. Taken together, our data suggest that Fliz1 plays a role in regulating thymocyte homeostasis.