Monday, 27 July 2015

CD52 depletion inhibits EAE

Turner MJ, Pang PT, Chretien N, Havari E, LaMorte MJ, Oliver J, Pande N, Masterjohn E, Carter K, Reczek D, Brondyk W, Roberts BL, Kaplan JM, Siders WM. Reduction of inflammation and preservation of neurological function by anti-CD52 therapy in murine experimental autoimmune encephalomyelitis. J Neuroimmunol. 2015;285:4-12.

Alemtuzumab, a monoclonal antibody directed against human CD52, is used in the treatment of MS. To characterize the impact of anti-CD52 administration, a monoclonal antibody to mouse CD52 (anti-muCD52) was generated and evaluated in EAE mouse models of MS. A single course of anti-muCD52 provided a therapeutic benefit accompanied by a reduction in the frequency of autoreactive T lymphocytes and production of pro-inflammatory cytokines. Examination of the CNS revealed a decrease in infiltrating lymphocytes, demyelination and axonal loss. Electrophysiological assessment showed preservation of axonal conductance in the spinal cord. These findings suggest that anti-CD52 therapy may help preserve CNS integrity.


So depletion of  CD52 expressing cells inhibits EAE....This in not surprising as depletion of CD4 T cells inhibits EAE.

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