New research has revealed how malaria parasites cause an inflammatory reaction that sabotages our body's ability to protect itself against the disease.Researchers from Melbourne's Walter and Eliza Hall Institute discovered that the same inflammatory molecules that drive the immune response in clinical and severe malaria also prevent the body from developing protective antibodies against the parasite.The discovery opens up the possibility of improving new or existing malaria vaccines by boosting key immune cells needed for long-lasting immunity.With many infections, a single exposure to the pathogen is enough to induce production of antibodies that will protect you for the rest of your life."However with malaria it can take up to 20 years for someone to build up sufficient immunity to be protected.
During that time people exposed to malaria are susceptible to re-infection and become sick many times, as well as spreading the disease," said lead researcher Diana Hansen.Malaria has traditionally been difficult to manage because the body is not good at developing long-lasting immunity to the parasite, which has hampered vaccine development, Hansen said."This was complicated by the fact that we didn't know whether it was the malaria parasite itself or the inflammatory reaction to malaria that was actually inhibiting the ability to develop protective immunity," the researcher explained."We have now shown that it was a double-edged sword: the strong inflammatory reaction that accompanies and in fact drives severe clinical malaria is also responsible for silencing the key immune cells needed for long-term protection against the parasite," Hansen added.
Co-lead researcher Axel Kallies said inflammatory molecules released by the body to fight the infection were preventing protective antibodies from being made."During malaria infection critical inflammatory molecules actually arrest development of helper T cells and therefore the B cells don't get the necessary instructions to make antibodies," he said.
The findings were published in the journal Cell Reports.