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This Article Figures Only Full Text Full Text (PDF) All Versions of this Article: 01.wnl.0000192109.81449.7av1 66/1_suppl_1/S59    most recent Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by McGavern, D. B. Search for Related Content PubMed PubMed Citation Articles by McGavern, D. B.

Immunotherapeutic relief from persistent infections and amyloid disorders

From the Division of Virology, Department of Neuropharmacology, The Scripps Research Institute, La Jolla, CA.

Address correspondence and reprint requests to Dr. Dorian B. McGavern, 10550 North Torrey Pines Rd., La Jolla, CA 92037; email: mcgad{at}scripps.edu

Persistent infections and amyloid disorders afflict a significant number of people worldwide. It would appear at first glance that the treatment of these afflictions should be entirely unrelated; however, in both cases components of the adaptive immune system have been harnessed in an attempt to provide some therapeutic relief. Given that the ability of a pathogen to establish persistence often depends in part on a shortcoming of the adaptive immune response, it seems logical to devise immunotherapies with the intention of supplementing (or replacing) the insufficient immunologic element. A case in point is an intervention referred as immunocytotherapy, which relies upon the adoptive transfer of pathogen-specific T lymphocytes into a persistently infected host. Remarkably, the adoptively transferred T lymphocytes not only have the capacity to clear the persistent infection, but can also provide the recipient with protection against subsequent rechallenge (i.e., immunologic memory). Treatment of amyloid disorders (e.g., Alzheimer disease, sporadic inclusion-body myositis) with a similar therapeutic approach is complicated by the fact that the aberrant protein accumulations are self-derived. Focusing the adaptive response on these aberrant self-proteins has the potential to result in autoimmune pathology. This review critically evaluates the importance of immunotherapeutic approaches for the treatment of persistent infections and amyloid disorders, and attempts to delineate the interventions that are most likely to succeed in an exceedingly complex disorder such as sporadic inclusion-body myositis.

This article was previously published in electronic format as an Expedited E-Pub at www.neurology.org.

Disclosure: The author reports no conflicts of interest.

Received June 22, 2005. Accepted in final form October 14, 2005.