Abstract
Experimental autoimmune encephalomyelitis (EAE) is the most relevant animal model to study demyelinating diseases such as multiple sclerosis. EAE can be induced by active (active EAE) or passive (at-EAE) transfer of activated T cells in several species and strains of rodents. However, histological features of at-EAE model in C57BL/6 are poorly described. The aim of this study was to characterize the neuroinflammatory and neurodegenerative responses of at-EAE in C57BL/6 mice by histological techniques and compare them with that observed in the active EAE model. To develop the at-EAE, splenocytes from active EAE female mice were harvested and cultured in presence of MOG35–55 and IL-12, and then injected intraperitoneally in recipient female C57BL6/J mice. In both models, the development of EAE was similar except for starting before the onset of symptoms and presenting a higher EAE cumulative score in the at-EAE model. Spinal cord histological examination revealed an increased glial activation as well as more extensive demyelinating areas in the at-EAE than in the active EAE model. Although inflammatory infiltrates composed by macrophages and T lymphocytes were found in the spinal cord and brain of both models, B lymphocytes were significantly increased in the at-EAE model. The co-localization of these B cells with IgG and their predominant distribution in areas of demyelination would suggest that IgG-secreting B cells are involved in the neurodegenerative processes associated with at-EAE.
Highlights
Experimental autoimmune encephalomyelitis (EAE) is a CD4+ T cell-mediated inflammatory demyelinating disease of the central nervous system (CNS)
Clinical Development of the adoptive transfer (at-EAE) Mice injected with MOG35–55 activated T cells developed the first neurological symptoms at day 8 reaching 100% of incidence on day (Figure 1A, C), while in the active EAE neurological symptoms starting two days later and reaching 100% of incidence on day (Figure 1B, C)
The loss of weight in the at-EAE animals occurred at the same time of the first clinical symptoms, while in the active
Summary
Experimental autoimmune encephalomyelitis (EAE) is a CD4+ T cell-mediated inflammatory demyelinating disease of the central nervous system (CNS). There is a great heterogeneity in the susceptibility and method of induction, in the response to immunological or neuropharmacological interventions [1,2,3] This makes EAE a very versatile system to use in translational neuroimmunopharmacology, but the model needs to be tailored to the scientific question being asked. The encephalitogenic T cells can be manipulated in vitro to study the role of specific cytokines and other biological agents before transfer to recipients. The at-EAE model is of particular interest to study the role of a variety of inflammatory molecules in different aspects of disease development and regulation through the use of gene-targeted donor or recipient animal strains [1,2]
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