| Affiliation: | (1) Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children Northern California, Sacramento, California USA, 95817;(2) Department of Dermatology, School of Medicine, University of California, Davis Sacramento, California, USA, 95816;(3) The Department of Neurology, School of Medicine, University of California Davis, Sacramento, California USA, 95817 |
| Abstract: | Background Murine experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis, presents typically as ascending paralysis. However, in mice in which interferon-gamma (IFNγ) signaling is disrupted by genetic deletion, limb paralysis is accompanied by atypical deficits, including head tilt, postural imbalance, and circling, consistent with cerebellar/vestibular dysfunction. This was previously attributed to intense cerebellar and brainstem infiltration by peripheral immune cells and formation of neutrophil-rich foci within the CNS. However, the exact mechanism by which IFNγ signaling prohibits the development of vestibular deficits, and whether the distribution and composition of inflammatory foci within the CNS affects the course of atypical EAE remains elusive. |
