Japanese Encephalitis Virus Induce Immuno-Competency in Neural Stem/Progenitor Cells (original) (raw)
Figure 6
Schematic representation of the possible role of NSPCs in induction of an immune response to virus infection.
Following JEV infection, NSPCs secrete an array of cyto/chemokines which help in the generation of an innate immune response against the viral pathogen. IFN-γ and IL-6 released form JEV infected NSPCs serve to activate the astrocytes and microglia, the primary immune cells of the CNS. Furthermore, both TNF-α and CCL2 have proven roles in upregulation of cell adhesion molecules on the endothelial cells of the blood brain barrier. These cell adhesion molecules help in recruitment of the activated T cells and monocytes from the periphery, which can now easily enter the CNS. On the other hand, JEV infection leads to upregulation of surface expression of costimulatory molecules like CD40, CD80, CD86 as well as MHC class I antigens on NSPCs. These costimulatory molecules and MHC class I on NSPCs are capable of providing functional co-stimulation to T cells and promote their proliferation. Furthermore, infected NSPCs also produce IL-2 which provides mitogenic signals for T cell proliferation. Thus, infected NSPCs are capable of stimulating the adaptive immune system, but whether the formation of an immunological synapse with T cells occurs is still under investigation.