Deletion of the complement anaphylatoxin C3a receptor attenuates, whereas ectopic expression of C3a in the brain exacerbates, experimental autoimmune encephalomyelitis. [electronic resource]
Producer: 20041115Description: 4708-14 p. digitalISSN:- 0022-1767
- Animals
- Brain -- immunology
- Cell Movement -- genetics
- Cells, Cultured
- Complement C3a -- biosynthesis
- Encephalomyelitis, Autoimmune, Experimental -- genetics
- Gene Deletion
- Glial Fibrillary Acidic Protein -- genetics
- Glycoproteins -- administration & dosage
- Humans
- Membrane Proteins -- biosynthesis
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Mice, Transgenic
- Myelin Sheath -- pathology
- Myelin-Oligodendrocyte Glycoprotein
- Peptide Fragments -- administration & dosage
- Receptors, Complement -- biosynthesis
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Publication Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
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