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. Author manuscript; available in PMC: 2014 Jul 23.
Published in final edited form as: J Clin Immunol. 2010 May;30(0 1):S50–S55. doi: 10.1007/s10875-010-9406-5

Fig. 3. rHIgM22, a recombinant human IgM, promotes remyelination of spinal cord demyelination.

Fig. 3

Light photomicrographs of normal spinal cord white matter showing densely packed myelinated axons (A). A typical demyelinated lesion with minimal remyelination as observed in the spinal cord of a susceptible mouse infected with Theiler’s murine encephalomyelitis virus for 5 months. This mouse was treated five weeks earlier with a control human IgM that does not bind to the surface of oligodendrocytes. The area contains only a few remyelinated axons. Infiltrating macrophages in the demyelinating lesion are characterized by the presence of darkly stained debris-laden vesicles (B). In contrast, much remyelination is observed in areas of chronic spinal cord demyelination of mice treated with rHIgM22, a recombinant human IgM that binds to myelin and the surface of oligodendrocytes (C). An area of nearly complete remyelination is present in the ventral lateral spinal cord after a single 50 μg dose intraperitoneally of rHIgM22 five weeks earlier. Remyelination is characterized by densely packed thin myelin sheaths in relation to axon diameter. Panels A, B and C are the same magnification.