Abstract
The murine anti-CD52 antibody, an equivalent of the humanized antibody alemtuzumab, which is successfully used in the treatment of multiple sclerosis, was used to explore a potential neuroprotective effect driven by immune cell derived brain-derived neurotrophic factor (BDNF). Therefore, lineage specific constitutive knock-out mice with a BDNF deficiency in T cells and macrophages were used and compared to treated wildtype mice. Neither therapeutic nor preventive application of the murine anti-CD52 antibody in an animal model of multiple sclerosis, the MOG35–55 EAE, revealed a beneficial contribution of immune cell derived BDNF to the disease outcome. Furthermore, preventive application of the murine anti-CD52 antibody worsened the clinical EAE disease course and could only be overcome by a prolonged recovery phase after treatment and before disease induction.
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