Effects of Brain-Derived IL-2 Deficiency and the Development of Autoimmunity on Spatial Learning and Fear Conditioning

Copyright: © 2015 Petitto J, 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. Interleukin-2 (IL-2) has been implicated in neurological disorders including multiple sclerosis and Alzheimer’s disease. Peripheral IL-2 deficiency in gene-deleted mice results in T cell mediated autoimmunity that begins to develop slowly after weaning and progressively increases through adulthood. Loss of brain-derived IL-2 results in neurobiological and behavioral abnormalities, and may contribute to the development of CNS autoimmunity by modifying the neuroimmunological milieu of the brain. We have shown previously that IL-2 knockout (KO) mice have altered learning acquisition in the Morris water-maze. Hypothesizing that the learning acquisition deficits in IL-2KO would be associated largely with the loss of brain-derived IL-2, the present study sought to determine if these cognitive alterations are due to the loss the IL-2 gene in the brain and/or autoimmunity resulting from loss of the gene in the peripheral immune system. We found that SCID congenic mice (mice free of IL-2 deficiency induced peripheral autoimmunity) without brain IL-2 (two IL-2KO alleles) did not differ from SCID congenic mice with normal brain IL-2 (two WT IL-2 alleles); thus, contrary to our hypothesis, loss of brain-derived IL-2 did not affect learning acquisition in the water-maze. Compared to adult WT littermates (9 weeks), adult IL-2KO mice with autoimmunit