In a study funded by the Wellcome Trust, Owain Millington and colleagues from the University of Strathclyde, UK, studied the effects of Plasmodium chabaudi, the mouse Plasmodium, on mice antigen-presenting dendritic cells in culture and confirmed their findings in live mice.
Millington et al.'s results show that dendritic cells exposed to P. chabaudi–infected red blood cells do not activate normally. They express lower levels of membrane molecules that stimulate other cells of the immune system, and their cytokine production is lower than that of normal dendritic cells. Millington et al. demonstrate that this is caused by exposure to hemozoin present in infected red blood cells.
Millington et al. then show that P.chabaudi-infected dendritic cells fail to activate helper T cells properly – T cells are activated but show reduced proliferation and cytokine production in culture. Importantly, during malaria infection, T cells fail to migrate to B-cell areas of lymph nodes or spleen, and this results in the failure of B-cell activation and antibody production.
Suppression of adaptive immunity to heterologous antigens during plasmodium infection through haemozoin-induced failure of DC function
Owain R Millington, Caterina Di Lorenzo, R Stephen Phillips, Paul Garside & James M Brewer
Journal of Biology 2006,5:5 (12 April 2006)
Last reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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