ED2-positive perivascular phagocytes produce interleukin-1β during delayed neuronal loss in the facial nucleus of the rat
✍ Scribed by D.N. Angelov; M. Walther; M. Streppel; O. Guntinas-Lichius; A.-M. van Dam; E. Stennert; W.F. Neiss
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 286 KB
- Volume
- 54
- Category
- Article
- ISSN
- 0360-4012
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✦ Synopsis
Injection of Fluoro-Gold (FG) into the whisker pad of rats yields stable retrograde labeling of facial motoneurons. Subsequent removal of 10 mm from all facial nerve branches permanently deprives the FG-labeled motoneurons from their targets and the motoneurons gradually die. Neuronal debris is phagocytized by two types of neuronophages: parenchymal microglia (monoclonal antibody [MAb] OX42-positive, MAb ED2-negative) and perivascular phagocytes (OX42negative, ED2-positive). Because both types of neuronophages express major histocompatibility complex (MHC) class II glycoproteins (MAb OX6-positive), they are considered to be the potential antigenpresenting cells of the brain. To check this hypothesis, we tested whether both types of neuronophages also synthetize the co-stimulatory cytokine interleukin-1 (IL-1) immunocytochemically visualized by MAbs SILK-5/6. Employing combined fluorescent visualization of antigens (OX6, ED2, and SILK-5/6) in sections containing fluorescent (FG-prelabeled) neuronophages, we found that, during slowly occurring neuronal loss, the vast majority of IL-1 immunoreactive neuronophages were of perivascular (ED2-positive) origin. We concluded that, during delayed neuronal death ''behind'' an intact blood-brain barrier, the perivascular phagocytes were more likely to function as antigenpresenting cells than the parenchymal microglia. J.