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Fig. 5 | Acta Neuropathologica Communications

Fig. 5

From: Retinal pathology in experimental optic neuritis is characterized by retrograde degeneration and gliosis

Fig. 5

A strong inflammatory response was observed in the optic nerve and retina of EAE mice. a T-cells (CD3) initially appear 11 days post immunisation (dpi) along with the cellular infiltration (DAPI), subsiding at later time points but still remaining until 33 dpi in the optic nerve of EAE mice. b T-cells were not observed in the retina of EAE mice at any time point. Yet, c Tnf expression amplified from 20 to 33 dpi in EAE compared to healthy controls in the retina. Tnf is a proinflammatory cytokine involved in the innate immune response. Whereas, d mRNA expression of Mcp1 in the retina increased significantly between 15 dpi and 28 dpi in EAE mice. Mcp1 likely plays an amplifying role (rather than an initiating role) in EAE. e Caspase 1 (Casp1) increases significantly from 15 dpi to 33 dpi in EAE retinas. It has a crucial role in development of immune mediated inflammatory processes leading to central nervous system demyelination. However, f Il-1β, which is a cytokine activated by Caspase 1, was not different in retinal expression between EAE mice and healthy controls. p-values for comparison between EAE and control mice (**** p < 0.00001, *** p < 0.0001, ** p < 0.01). EAE: experimental autoimmune encephalomyelitis, TNF: tumor necrosis factor, MCP1: monocyte chemoattractant protein 1, IL-1β: interleukin-1β, IRL: inner retinal layer, INL: inner nuclear layer, ONL: outer nuclear layer. EAE: experimental autoimmune encephalomyelitis, IBA1: allograft inflammatory factor 1, TMEM119: transmembrane protein 119, IRL: inner retinal layer, INL: inner nuclear layer, ONL: outer nuclear layer

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