[ORIGINAL CONTRIBUTIONS]Impaired Th2 differentiation of CD4+ T cells from Rap2b knockout mice
| Autor: | Uechi, Yukiko, Matsuzaki, Goro, Suzuki, Masako, Asato, Tsuyoshi, Takei, Kimiko, Umikawa, Masato, Oshiro, Minoru, Maruyama, Ichiro N, Endo, Shogo, Kariya, Ken-ichi |
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| Jazyk: | angličtina |
| Předmět: | |
| Zdroj: | 琉球医学会誌 = Ryukyu Medical Journal. 34(1･2):45-52 |
| ISSN: | 1346-888X |
| Popis: | Rap1 and Rap2 are Ras-like small G proteins. Rap1 plays major roles in embryogenesis and in hematopoietic systems, as demonstrated by gene knockout studies. On the other hand, Rap2 functions had been unclear until we identified its effectors, protein kinases upstream of c-Jun N-terminal kinase (JNK), the stress-activated mitogen-activated kinase (MAPK). Herein, we report the first gene knockout study of Rap2. Rap2b-null mutant (Rap2b–/–) mice were viable and showed no overt abnormalities in the development or homing of hematopoietic cells. Rap2b–/– CD4+ T cells exhibited MAPK activation patterns comparable to those of Rap2b+/+ counterparts upon acute T-cell receptor (TCR) stimulation. Both Rap2b–/– CD4+ T cells and Rap2b+/+ counterparts secreted similar amounts of IFN-γ upon TCR restimulation after growth under T helper 1 (Th1) polarizing condition. However, secretion of IL-4, IL-5 and IL-13 from Th2-conditioned Rap2b–/– cells was half that of Rap2b+/+ counterparts, suggesting impaired Th2 polarization. Notably, sorted Rap2b–/– CD62Lhigh CD4+ T cells, consisting mainly of naïve cells, showed normal Th2 polarization. By contrast, Rap2b–/– CD62Llow CD4+ T cells showed impaired Th2 polarization, potentially accounting for the abnormality of unsorted Rap2b–/– CD4+ T cells. Impaired Th2 polarization has not previously been reported in Rap-related genetic models and requires further investigation. 論文 |
| Databáze: | OpenAIRE |
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