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. Author manuscript; available in PMC: 2019 Sep 6.
Published in final edited form as: Annu Rev Immunol. 2019 Apr 26;37:73–95. doi: 10.1146/annurev-immunol-042718-041417

Figure 1.

Figure 1

CNS-resident and peripheral immune responses promote antiviral and immunopathogenic outcomes. Activation of CNS-resident neurons and glia, either directly by viral-sensing PRRs or indirectly, promotes antiviral and inflammatory cytokine expression and leads to restriction and resolution of viral infection. Prolonged glia activation additionally may initiate neuropathogenic programs. The innate immune response of CNS-resident cells also shapes the recruitment and activation of peripheral immune cells through the expression of chemokines, modulation of the BBB, and cell-cell interaction (not shown). Infiltration of immune cells is critical for viral clearance and establishment of long-term protection in the CNS, but it may facilitate neuroinvasion or contribute to neuropathology both during and after infection. Antiviral and immunopathogenic outcomes are labeled blue and red, respectively. Abbreviations: BBB, blood-brain barrier; BMEC, brain microvascular endothelial cell; CNS, central nervous system; PRR, pattern recognition receptor; Treg, regulatory T cell; Trm, tissue-resident memory T cell.