Altered cellular immunity in transgenic mice with T cell-specific expression of human D4-guanine diphosphate-dissociation inhibitor (D4-GDI)
International Immunology, ISSN: 0953-8178, Vol: 20, Issue: 10, Page: 1299-1311
2008
- 3Citations
- 13Captures
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Metrics Details
- Citations3
- Citation Indexes3
- CrossRef3
- Captures13
- Readers13
- 13
Article Description
D4-GDI, a Rho guanosine diphosphate (GDP) dissociation inhibitor, is preferentially expressed in hematopoietic tissues and binds to a small GTP-binding protein, Rho, and inhibits GDP dissociation from Rho. We identified point mutations in the D4-GDI gene in human leukemic cells. We therefore investigated the functions of D4-GDI and mutated D4-GDI in T cells. Transgenic mice (Tg) harboring human wild-type and mutant D4-GDI transgenes driven by the lck promoter were generated. Cellular immunity responses against cytozoic pathogens were examined. The cytoskeletal organization in the CD3+T cells and the proliferation of splenocytes by Con A were investigated in both Tg and littermates (LMs). Granuloma formation by bacille Calmette-Guerin was impaired in the wild-type D4-GDI Tg. On the other hand, the number of granulomas of the mutated D4-Tg was significantly higher. Infection with Listeria was more rapidly fatal to wild-type D4-GDI Tg than to LMs, while the survival of mutated D4-GDI Tg was prolonged. The CD3+T cells in wild-type D4-GDI Tg showed an impairment in the formation of stress fibers on anti-CD3 antibody-coated plates, whereas the cytoskeletal organization in CD3+T cells of the mutated D4-GDI Tg was augmented. The proliferation of splenocytes after Con A stimulation was higher in the mutated D4-GDI Tg than in the LMs. D4-GDI may have important functions, such as induction of T cell migration, adhesion and/or proliferation in inflammatory foci, in cellular immunity responses to cytozoic pathogens. © 2008 The Japanese Society for Immunology. 2008. All rights reserved.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=52949124867&origin=inward; http://dx.doi.org/10.1093/intimm/dxn084; http://www.ncbi.nlm.nih.gov/pubmed/18689726; https://academic.oup.com/intimm/article-lookup/doi/10.1093/intimm/dxn084; https://dx.doi.org/10.1093/intimm/dxn084; https://academic.oup.com/intimm/article-abstract/20/10/1299/700037?redirectedFrom=fulltext
Oxford University Press (OUP)
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