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Background  MicroRNAs (miRNAs) are noncoding RNAs that modulate cellular gene expression, primarily at the post-transcriptional level. We sought to examine the functional role of miR-155 in a model of viral-induced neuroinflammation.    Methods  Acute encephalomyelitis and immune-mediated demyelination were induced by intracranial injection with the neurotropic JHM strain of mouse hepatitis virus (JHMV) into C57BL/6  miR-155   +/+   wildtype (WT) mice or  miR-155   −/−   mice. Morbidity and mortality, viral load and immune cell accumulation in the CNS, and spinal cord demyelination were assessed at defined points post-infection. T cells harvested from infected mice were used to examine cytolytic activity, cytokine activity, and expression of certain chemokine receptors. To determine the impact of miR-155 on trafficking, T cells from infected WT or  miR-155   −/−   mice were adoptively transferred into  RAG1   −/−   mice, and T cell accumulation into the CNS was assessed using flow cytometry. Statistical significance was determined using the Mantel-Cox log-rank test or Student’s  T  tests.    Results  Compared to WT mice, JHMV-infected  miR-155   −/−   mice developed exacerbated disease concomitant with increased morbidity/mortality and an inability to control viral replication within the CNS. In corroboration with increased susceptibility to disease,  miR-155   −/−   mice had diminished CD8 +  T cell responses in terms of numbers, cytolytic activity, IFN-γ secretion, and homing to the CNS that corresponded with reduced expression of the chemokine receptor CXCR3. Both IFN-γ secretion and trafficking were impaired in  miR-155   −/−  , virus-specific CD4 +  T cells; however, expression of the chemokine homing receptors analyzed on CD4 +  cells was not affected. Except for very early during infection, there were not significant differences in macrophage infiltration into the CNS between WT and  miR-155   −/−   JHMV-infected mice, and the severity of demyelination was similar at 14 days p.i. between WT and  miR-155   −/−   JHMV-infected mice.    Conclusions  These findings support a novel role for miR-155 in host defense in a model of viral-induced encephalomyelitis. Specifically, miR-155 enhances antiviral T cell responses including cytokine secretion, cytolytic activity, and homing to the CNS in response to viral infection. Further, miR-155 can play either a host-protective or host-damaging role during neuroinflammation depending on the disease trigger.

MicroRNA-155 enhances T cell trafficking and antiviral effector function in a model of coronavirus-induced neurologic disease