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- Title
Gimap3 and Gimap5 cooperate to maintain T-cell numbers in the mouse.
- Authors
Yano, Kouta; Carter, Christine; Yoshida, Naofumi; Abe, Takaya; Yamada, Akiko; Nitta, Takeshi; Ishimaru, Naozumi; Takada, Kensuke; Butcher, Geoffrey W.; Takahama, Yousuke
- Abstract
Gimap3 ( IAN4) and Gimap5 ( IAN5) are highly homologous GTP-binding proteins of the Gimap family. Gimap3 and Gimap5, whose transcripts are abundant in mature lymphocytes, can associate with antiapoptotic Bcl-2 family proteins. While it is established that Gimap5 regulates T-cell survival, the in vivo role of Gimap3 is unclear. Here we report the preparation and characteristics of mouse strains lacking Gimap3 and/or Gimap5. We found that the number of T cells was markedly reduced in mice deficient in both Gimap3 and Gimap5. The defects in T-cell cellularity were more severe in mice lacking both Gimap3 and Gimap5 than in mice lacking only Gimap5. No defects in the cellularity of T cells were detected in mice lacking only Gimap3, whereas bone marrow cells from Gimap3-deficient mice showed reduced T-cell production in a competitive hematopoietic environment. Moreover, retroviral overexpression and short hairpin RNAs-mediated silencing of Gimap3 in bone marrow cells elevated and reduced, respectively, the number of T cells produced in irradiated mice. These results suggest that Gimap3 is a regulator of T-cell numbers in the mouse and that multiple Gimap family proteins cooperate to maintain T-cell survival.
- Publication
European Journal of Immunology, 2014, Vol 44, Issue 2, p561
- ISSN
0014-2980
- Publication type
Article
- DOI
10.1002/eji.201343750