Anti-myelin basic protein

Bansal, G., Martenson, R. E., Leveille, P., and Campagnoni, A. T. (1987) Characterization of a novel monoclonal anti-myelin basic protein antibody use in immunoblotting and immunohistochemical studies. J. Neuroimmunol. 15, 279-294. 

Mostafa GA, Al-Ayadhi LY. A lack of association between hyperserotonemia and the increased frequency of serum anti-myelin basic protein auto-antibodies in autistic children. / Neuroinflammation. 2011 8 71. 

Figure 44.3. T cell-mediated neui oprotecdon in a PD model. In MPTP-intoxicated mice, regulatory T cells infiltrate tire inflamed nigrostiiatal patliway where tliey encounter cross-reactive CNS antigens (such as myelin basic protein or reactive species-modified proteins) presented in tire context of MHC by resident microglial cells. In response, activated T cells secrete anti-inflammatory cytokines such as IL-4, IL-10, and TGF- 3 tliat suppress toxic microglial activities. Neurotrophin expression may occur directly from T cells or T cell-derived IL-4, and IL-10 may induce neurotrophin production in neigliboimg glia. Tliese activities lead to neuroprotection indirectly by suppression of microglial responses and directly tlu ough tire local delivery of neurotropliins.

Notest aData for compounds 3 and 4 taken from ref. 263 data for compound 10 taken from ref. 266. bRats with lesioned sciatic nerves were treated with the indicated compounds, and sacrificed on the 18th day of the experiment. Axonal diameter and cross-sectional area were quantitated by anti-neurofilament staining, and myelin levels were quantitated by myelin basic protein-immunoreactive stain density. 

Capture and primary antibody Mouse anti-human phosphorylated myelin basic protein (MBP) (US Biological, MA) (see Note 3). 

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