The Yale research team learned that the 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 Yale 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,” said Rick Bucala, M.D., 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.”
More information: PNAS paper: www.pnas.org/conte… ull.pdf+html