PI3Kδ drives the pathogenesis of experimental autoimmune encephalomyelitis by inhibiting effector T cell apoptosis and promoting Th17 differentiation.

MLA

Haylock-Jacobs, Sarah, et al. “PI3Kδ Drives the Pathogenesis of Experimental Autoimmune Encephalomyelitis by Inhibiting Effector T Cell Apoptosis and Promoting Th17 Differentiation.” Journal of Autoimmunity, vol. 36, no. 3–4, May 2011, pp. 278–87. EBSCOhost, https://doi.org/10.1016/j.jaut.2011.02.006.

APA

Haylock-Jacobs, S., Comerford, I., Bunting, M., Kara, E., Townley, S., Klingler-Hoffmann, M., Vanhaesebroeck, B., Puri, K. D., & McColl, S. R. (2011). PI3Kδ drives the pathogenesis of experimental autoimmune encephalomyelitis by inhibiting effector T cell apoptosis and promoting Th17 differentiation. Journal of Autoimmunity, 36(3–4), 278–287. https://doi.org/10.1016/j.jaut.2011.02.006

Chicago

Haylock-Jacobs, Sarah, Iain Comerford, Mark Bunting, Ervin Kara, Scott Townley, Manuela Klingler-Hoffmann, Bart Vanhaesebroeck, Kamal D Puri, and Shaun R McColl. 2011. “PI3Kδ Drives the Pathogenesis of Experimental Autoimmune Encephalomyelitis by Inhibiting Effector T Cell Apoptosis and Promoting Th17 Differentiation.” Journal of Autoimmunity 36 (3–4): 278–87. doi:10.1016/j.jaut.2011.02.006.