Immunoglobulin-M
(IgM) monoclonal antibodies that bind to oligodendrocytes also appear to
induce remyelination. In 2003, a patent was granted for the use
of some of these antibodies, in particular SCH 94.03, for "diagnostic and
therapeutic uses...in the central nervous system" [8].
In 1998,
several different antibodies were tested to see if they could promote
remyelination in the central nervous system. Panels A-E of Figure 3
(below) show signs of remyelination when treated with oligodendrocyte-reactive
antibodies SCH79.08 (A), O1 (B), O4 (C), A2B5 (D), and HNK-1 (E). However,
antibodies of class Immunoglobulin-M that do not bind to oligodendrocytes, in
particular R24 (F), CH12 (G), and ABPC22 (H), do not induce any significant
remyelination [9].
However, one
of the best performers for remyelination is HIgM22. Just one
500-nanogram injection of a recombinant form of this monoclonal
antibody was recently shown to induce remyelination within five weeks,
despite the antibody being nearly completely eliminated from the body within 24
hours [10].
In Figure 4 (above), each
picture was taken five weeks after injection with either a
phosphate-buffered saline control (A) or recombinant HIgM22 (B,C). 4C
is a higher magnification of the asterisked area in 4B. The presence of
some remyelination in 4A indicates that a minimal level of remyelination can
occur in the absence of any external factors. However, myelination is far
further along in 4B, and even better exemplified by the higher magnification
picture in 4C.
The use of recombinant human IgM antibodies that
bind oligodendrocytes is another antibody-based potential
demyelination therapy that holds great promise.
