Interleukin-13 and its receptor are synaptic proteins involved in plasticity and neuroprotection. Nat Commun 2023 Jan 13;14(1):200
Date
01/14/2023Pubmed ID
36639371Pubmed Central ID
PMC9839781DOI
10.1038/s41467-023-35806-8Scopus ID
2-s2.0-85146272971 (requires institutional sign-in at Scopus site) 12 CitationsAbstract
Immune system molecules are expressed by neurons, yet their functions are often unknown. We have identified IL-13 and its receptor IL-13Ra1 as neuronal, synaptic proteins in mouse, rat, and human brains, whose engagement upregulates the phosphorylation of NMDAR and AMPAR subunits and, in turn, increases synaptic activity and CREB-mediated transcription. We demonstrate that increased IL-13 is a hallmark of traumatic brain injury (TBI) in male mice as well as in two distinct cohorts of human patients. We also provide evidence that IL-13 upregulation protects neurons from excitotoxic death. We show IL-13 upregulation occurring in several cohorts of human brain samples and in cerebrospinal fluid (CSF). Thus, IL-13 is a physiological modulator of synaptic physiology of neuronal origin, with implications for the establishment of synaptic plasticity and the survival of neurons under injury conditions. Furthermore, we suggest that the neuroprotection afforded through the upregulation of IL-13 represents an entry point for interventions in the pathophysiology of TBI.
Author List
Li S, Olde Heuvel F, Rehman R, Aousji O, Froehlich A, Li Z, Jark R, Zhang W, Conquest A, Woelfle S, Schoen M, O Meara CC, Reinhardt RL, Voehringer D, Kassubek J, Ludolph A, Huber-Lang M, Knöll B, Morganti-Kossmann MC, Brockmann MM, Boeckers T, Roselli FAuthor
Caitlin C. O'Meara PhD Associate Professor in the Physiology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBrain Injuries, Traumatic
Humans
Interleukin-13
Male
Mice
Neuronal Plasticity
Neurons
Neuroprotection
Rats
