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Blood, 1 September 2005, Vol. 106, No. 5, pp. 1676-1684. Prepublished online as a Blood First Edition Paper on May 12, 2005; DOI 10.1182/blood-2004-10-4047. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-10-4047v1 106/5/1676    most recent Alert me when this article is cited 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 Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Stephens, R. Articles by Langhorne, J. Search for Related Content PubMed PubMed Citation Articles by Stephens, R. Articles by Langhorne, J. Related Collections Immunobiology Red Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Malaria-specific transgenic CD4+ T cells protect immunodeficient mice from lethal infection and demonstrate requirement for a protective threshold of antibody production for parasite clearance Robin Stephens, Frank R. Albano, Stuart Quin, Benjamin J. Pascal, Vicky Harrison, Brigitta Stockinger, Dimitris Kioussis, Hans-Ulrich Weltzien, and Jean Langhorne From the Division of Parasitology, National Institute of Medical Research, The Ridgeway, Mill Hill, London, United Kingdom; Division of Molecular Immunology, National Institute of Medical Research, The Ridgeway, Mill Hill, London, United Kingdom; and Max Planck Institute for Immunobiology, Freiburg, Germany. T cells are important in the immune response to malaria, both for their cytokines and their help for antibody production. To look at the relative importance of these roles, a T-cell receptor (TCR) transgenic mouse has been generated carrying a TCR specific for an epitope of the merozoite surface protein 1 (MSP-1) of the malaria parasite, Plasmodium chabaudi. In adoptive transfer experiments, malaria-specific CD4+ T cells expand and produce interferon (IFN-) early in infection, but the population contracts quickly despite prolonged persistence of the parasite. MSP-1-specific CD4+ cells can protect immunodeficient mice from lethal infection; however, the parasite is only completely cleared in the presence of B cells showing that T helper cells are critical. Levels of malaria-specific antibody and the speed of their production clearly correlate with the time of resolution of infection, indicating that a critical threshold of antibody production is required for parasite clearance. Furthermore, T cells specific for a shed portion of MSP-1 are able to provide help for antibody to the protective region, which remains bound to the infected erythrocyte, suggesting that MSP-1 has all of the components necessary for a good vaccine. (Blood. 2005;106:1676-1684) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A.-M. Sponaas, E. T. Cadman, C. Voisine, V. Harrison, A. Boonstra, A. O'Garra, and J. Langhorne Malaria infection changes the ability of splenic dendritic cell populations to stimulate antigen-specific T cells J. Exp. Med., June 12, 2006; 203(6): 1427 - 1433. [Abstract] [Full Text] [PDF]

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