Loss of Neuronal Phenotype and neurodegeneration: Effects of T Lymphocytes and Brain Interleukin-2
Danielle Meola, Zhi Huang, Grace K Ha, and John M Petitto*
Departments of Psychiatry, Neuroscience, Pharmacology and Therapeutics, McKnight Brain Institute, University of Florida, Gainesville, FL, USA
- Corresponding Author:
- Dr. John M Petitto
Departments of Psychiatry, Neuroscience
Pharmacology and Therapeutics
McKnight Brain Institute
University of Florida
Gainesville, FL, USA
E-mail: [email protected]
Received date: December 18, 2012; Accepted date: January 16, 2013; Published date: January 25, 2013
Citation: Meola D, Huang Z, Ha GK, Petitto JM (2013) Loss of Neuronal Phenotype and Neurodegeneration: Effects of T Lymphocytes and Brain Interleukin-2. J Alzheimers Dis Parkinsonism S10:003. doi:10.4172/2161-0460.S10-003
Copyright: © 2013 Meola D, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Loss of neuronal phenotype and reversal of neuronal atrophy have been demonstrated in different models of central nervous system (CNS) injury. These processes may be generalizable to different types of brain neurons and circuitry. The idea that some injured neurons may lose their phenotype and/or atrophy with the potential to rejuvenate is a remarkable and potentially promising form of neuronal plasticity that is not well understood. In this paper, we present some of our laboratory’s basic neuroimmunology research showing that peripheral T cells entering the CNS, and brain-derived interleukin-2 (IL-2), play significant roles in these intriguing processes. Our findings suggest, for example, that T cell immunosenesence could be involved in related processes of brain aging and contribute to neurodegenerative disease. Neuroimmunological approaches may provide new insights into yet undiscovered factors and brain mechanisms that regulate changes in neuronal integrity associated with aging and disease. Such findings could have important implications for discovering more effective strategies for treating patients with neurotrauma and neurodegenerative diseases (e.g., Alzheimer’s disease).