| First Author | Zhang B | Year | 2016 |
| Journal | Immunity | Volume | 44 |
| Issue | 3 | Pages | 568-581 |
| PubMed ID | 26921109 | Mgi Jnum | J:258662 |
| Mgi Id | MGI:6140588 | Doi | 10.1016/j.immuni.2016.01.007 |
| Citation | Zhang B, et al. (2016) MicroRNA-23a Curbs Necrosis during Early T Cell Activation by Enforcing Intracellular Reactive Oxygen Species Equilibrium. Immunity 44(3):568-581 |
| abstractText | Upon antigen engagement, augmented cytosolic reactive oxygen species (ROS) are needed to achieve optimal T cell receptor (TCR) signaling. However, uncontrolled ROS production is a prominent cause of necrosis, which elicits hyper-inflammation and tissue damage. Hence, it is critical to program activated T cells to achieve ROS equilibrium. Here, we determined that miR-23a is indispensable for effector CD4(+) T cell expansion, particularly by providing early protection from excessive necrosis. Mechanistically, miR-23a targeted PPIF, gatekeeper of the mitochondria permeability transition pore, thereby restricting ROS flux and maintaining mitochondrial integrity. Upon acute Listeria monocytogenes infection, deleting miR-23a in T cells resulted in excessive inflammation, massive liver damage, and a marked mortality increase, which highlights the essential role of miR-23a in maintaining immune homeostasis. |
