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https://doi.org/10.1016/j.isci.2019.05.045
| Title: | Ap4A Regulates Directional Mobility and Antigen Presentation in Dendritic Cells | Authors: | La Shu, S. Paruchuru, L.B. Tay, N.Q. Chua, Y.L. Yun Foo, A.S. Yang, C.M. Liong, K.H. Liang Koh, E.G. Lee, A. Nechushtan, H. Razin, E. Kemeny, D.M. |
Keywords: | Immune Response Immunology Model Organism Molecular Mechanism of Behavior |
Issue Date: | 2019 | Publisher: | Elsevier Inc. | Citation: | La Shu, S., Paruchuru, L.B., Tay, N.Q., Chua, Y.L., Yun Foo, A.S., Yang, C.M., Liong, K.H., Liang Koh, E.G., Lee, A., Nechushtan, H., Razin, E., Kemeny, D.M. (2019). Ap4A Regulates Directional Mobility and Antigen Presentation in Dendritic Cells. iScience 16 : 524-534. ScholarBank@NUS Repository. https://doi.org/10.1016/j.isci.2019.05.045 | Rights: | Attribution-NonCommercial-NoDerivatives 4.0 International | Abstract: | The significance of intracellular Ap4A levels over immune activity of dendritic cells (DCs) has been studied in Nudt2fl/fl/CD11c-cre mice. The transgenic mice have been generated by crossing floxed NUDT2 gene mice with DC marker CD11c recombinase (cre) mice. The DCs derived from these mice have higher levels of Ap4A (?30-fold) compared with those derived from Nudt2+/+ mice. Interestingly, the elevated Ap4A in DCs has led them to possess higher motility and lower directional variability. In addition, the DCs are able to enhance immune protection indicated by the higher cross-presentation of antigen and priming of CD8+ OT-I T cells. Overall, the study denotes prominent impact of Ap4A over the functionality of DCs. The Nudt2fl/fl/CD11c-cre mice could serve as a useful tool to study the influence of Ap4A in the critical immune mechanisms of DCs. Molecular Mechanism of Behavior; Immunology; Immune Response; Model Organism © 2019 The Author(s) | Source Title: | iScience | URI: | https://scholarbank.nus.edu.sg/handle/10635/209962 | ISSN: | 2589-0042 | DOI: | 10.1016/j.isci.2019.05.045 | Rights: | Attribution-NonCommercial-NoDerivatives 4.0 International |
| Appears in Collections: | Elements Staff Publications |
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