| First Author | Aravalli RN | Year | 2005 |
| Journal | J Immunol | Volume | 175 |
| Issue | 7 | Pages | 4189-93 |
| PubMed ID | 16177057 | Mgi Jnum | J:118997 |
| Mgi Id | MGI:3700908 | Doi | 10.4049/jimmunol.175.7.4189 |
| Citation | Aravalli RN, et al. (2005) Cutting edge: TLR2-mediated proinflammatory cytokine and chemokine production by microglial cells in response to herpes simplex virus. J Immunol 175(7):4189-93 |
| abstractText | Recent studies indicate that TLRs are critical in generating innate immune responses during infection with HSV-1. In this study, we investigated the role of TLR2 signaling in regulating the production of neuroimmune mediators by examining cytokine and chemokine expression using primary microglial cells obtained from TLR2-/- as well as wild-type mice. Data presented here demonstrate that TLR2 signaling is required for the production of proinflammatory cytokines and chemokines: TNF-alpha, IL-1beta, IL-6, IL-12, CCL7, CCL8, CCL9, CXCL1, CXCL2, CXCL4, and CXCL5. CXCL9 and CXCL10 were also induced by HSV, but their production was not dependent upon TLR2 signaling. Because TLR2-/- mice display significantly reduced mortality and diminished neuroinflammation in response to brain infection with HSV, the TLR2-dependent cytokines identified here might function as key players influencing viral neuropathogenesis. |
