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. Author manuscript; available in PMC: 2019 Jun 1.
Published in final edited form as: J Neuroimmune Pharmacol. 2017 Nov 20;13(2):126–142. doi: 10.1007/s11481-017-9770-5

Figure 9.

Figure 9

Schematic presentation of the role of agnoprotein in neuroimmune response to JC virus. Infected cells set the stage of pro-inflammatory signaling to the bystander uninfected cells to initiate neuroinflammation induced by GM-CSF activation. Upon activation, GM-CSF can serve as a chemo-attractant for the migration of lymphocytes through blood-brain barrier into the area of infection and contribute to their maturation and differentiation within the brain. Agnoprotein is expressed and released into the extracellular space by cells infected with JC virus and taken up by uninfected bystander glial cells. Pro-inflammatory signaling between infected and uninfected cells leading to the GM-CSF activation and neuroinflammation is disrupted by extracellular and intracellular agnoprotein leading to the development of PML lesions.