| First Author | Chauhan P | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Pages | 41889 | PubMed ID | 28165503 |
| Mgi Jnum | J:275073 | Mgi Id | MGI:6296072 |
| Doi | 10.1038/srep41889 | Citation | Chauhan P, et al. (2017) Modulation of Microglial Cell Fcgamma Receptor Expression Following Viral Brain Infection. Sci Rep 7:41889 |
| abstractText | Fcgamma receptors (FcgammaRs) for IgG couple innate and adaptive immunity through activation of effector cells by antigen-antibody complexes. We investigated relative levels of activating and inhibitory FcgammaRs on brain-resident microglia following murine cytomegalovirus (MCMV) infection. Flow cytometric analysis of microglial cells obtained from infected brain tissue demonstrated that activating FcgammaRs were expressed maximally at 5 d post-infection (dpi), while the inhibitory receptor (FcgammaRIIB) remained highly elevated during both acute and chronic phases of infection. The highly induced expression of activating FcgammaRIV during the acute phase of infection was also noteworthy. Furthermore, in vitro analysis using cultured primary microglia demonstrated the role of interferon (IFN)gamma and interleukin (IL)-4 in polarizing these cells towards a M1 or M2 phenotype, respectively. Microglial cell-polarization correlated with maximal expression of either FcgammaRIV or FcgammaRIIB following stimulation with IFNgamma or IL-4, respectively. Finally, we observed a significant delay in polarization of microglia towards an M2 phenotype in the absence of FcgammaRs in MCMV-infected Fcer1g and FcgR2b knockout mice. These studies demonstrate that neuro-inflammation following viral infection increases expression of activating FcgammaRs on M1-polarized microglia. In contrast, expression of the inhibitory FcgammaRIIB receptor promotes M2-polarization in order to shut-down deleterious immune responses and limit bystander brain damage. |
