MOG (35-55) is a 35-55 fragment of myelin oligodendrocyte glycoprotein [1]. Immunizing mice with MOG (35-55) peptide to induce experimental autoimmune encephalomyelitis (EAE), it causes inflammation (macrophages and CD3+ T lymphocytes), demyelination, and axonal loss [1]. MOG (35-55) is often used to model EAE in mice for evaluating various drug treatments [2].
Axon loss in the medial dorsal column (fasciculus gracilis), which is often damaged in this model of EAE, was detected as early as 7 days post-immunization (p.i.), with a loss of about 11% of axons in the defined counting area. A further 10% loss was observed by day 12 p.i., at which time behavioral disease was just beginning to become apparent [1]. T lymphocytes were detected infiltrating the spinal cord as early as day 7 p.i. CD3-immunoreactivity increased 5-fold [1]. MOG (35-55) immunized mice developed severe parenchymal infiltration in the spinal cords on day 9, day 13 and day 16, and mice showed heavy infiltration of the cerebral meninges, which prevailed in the region of the hippocampus involving the lateral and the third ventricle [3]. MOG (35-55)-induced EAE showed the cerebellar white matter infiltrates in all mice on days 13 and 16 [3].
References:
[1]. Jones M V, Nguyen T T, Deboy C A, et al. Behavioral and pathological outcomes in MOG 35-55 experimental autoimmune encephalomyelitis[J]. Journal of neuroimmunology, 2008, 199(1-2): 83-93.
[2]. Steinman L, Zamvil S S. Virtues and pitfalls of EAE for the development of therapies for multiple sclerosis[J]. Trends in immunology, 2005, 26(11): 565-571.
[3]. Kuerten S, Kostova-Bales D A, Frenzel L P, et al. MP4-and MOG: 35-55-induced EAE in C57BL/6 mice differentially targets brain, spinal cord and cerebellum[J]. Journal of neuroimmunology, 2007, 189(1-2): 31-40.