Health & Medicine - Posted by Helen Dodson-Yale on Friday, July 13, 2012 11:37 - 0 Comments
How malaria outsmarts immune system memory
YALE (US) — The parasite that causes malaria creates its own version of a human immune hormone—a trick that keeps the body from remembering the infection and developing immunity.
One of the biggest problems in controlling malaria in regions of high transmission, where it continues to account for over one million deaths yearly, is that protective immunity against re-infection does not occur.
Straight from the Source
It is believed that inadequate formation and maintenance of infection-fighting memory T-cells are at the root of this immune malfunction. This phenomenon also frustrates efforts to develop effective malaria vaccines.
In addition, malaria causes a highly inflammatory response in infected individuals that leads to the deadly clinical complications of anemia and cerebral disease.
Now, a team of researchers from Yale University has learned that the mosquito-borne parasites produce their own version of a human cytokine, or immune hormone, which directs the inflammatory response during malaria. They also discovered that this cytokine, called PMIF, incapacitates the anti-malaria, memory T-cell immune response.
Using a genetically modified strain of the malaria parasite in mice, the team found that PMIF causes host T-cells to develop into short-lived effector cells rather than protective memory cells.
The short-lived cells die during the infection, and the long-lived memory T-cells are not produced in adequate numbers to combat the infection or to protect from re-infection, which occurs repeatedly in malaria-endemic regions.
“These findings indicate that malaria parasites actively interfere with the development of immunological memory, and may account for the inhibition of protective immune responses in human malaria,” says Rick Bucala, professor of internal medicine, pathology, and epidemiology and public health at Yale School of Medicine.
“This knowledge will help us identify specific therapies that can protect anti-malarial T-cells from death and improve an individual’s immune response to infection or to vaccination.”
The study, published in the Online Early Edition of the Proceedings of the National Academy of Sciences, is the graduate thesis of Tiffany Sun. Additional authors contributed from Yale, Mount Sinai School of Medicine, Howard University, the Malaria Institute at Macha in Zambia, and Leiden University in The Netherlands.
The research was supported by the National Science Foundation, the National Institutes of Health, and the Netherlands Organization for Scientific Research.
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