According to a report in today's Science, a productive approach to combating the spongiform encephalopathies such as the transmissible "variant" Creutzfeldt-Jacob disease (vCJD, popularly known as "mad cow disease") may be to attack cells in the spleen where the putative culprit, the prion protein, appears early in these diseases. Before vCJD produces clinical neurological symptoms, prions apparently replicate and accumulate in follicular dendritic cells in the spleen. Researchers in London, Zurich, and Cambridge, Massachusetts, have taken advantage of the fact that these particular cells need to interact with B lymphocytes via a signaling protein called lymphotoxin in order to mature and survive.

The researchers deactivated the lymphotoxin on B lymphocytes in mice that were exposed to scrapie, a spongiform encephalopathy of sheep, and found that follicular dendritic cell numbers were drastically reduced. Along this decline, prions stopped accumulating in the spleen and the mice developed scrapie much later than did control mice. The authors speculate that, if diagnosed early enough, diseases such as vCJD might be treatable with agents that inhibit the necessary interactions between B lymphocytes and follicular dendritic cells.—Hakon Heimer


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  1. . Impaired prion replication in spleens of mice lacking functional follicular dendritic cells. Science. 2000 May 19;288(5469):1257-9. PubMed.