| First Author | Yano K | Year | 2014 |
| Journal | Eur J Immunol | Volume | 44 |
| Issue | 2 | Pages | 561-72 |
| PubMed ID | 24510501 | Mgi Jnum | J:209926 |
| Mgi Id | MGI:5568914 | Doi | 10.1002/eji.201343750 |
| Citation | Yano K, et al. (2014) Gimap3 and Gimap5 cooperate to maintain T-cell numbers in the mouse. Eur J Immunol 44(2):561-72 |
| abstractText | 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. |
