A discovery about how the immune system responds to malaria infection could lead to better treatments for hepatitis C, HIV and lupus. The research showed, in laboratory models, that strong inflammatory signals caused by malaria infection activate molecules that trigger B cells to produce highly potent antibodies to fight the disease.
It found that infection with the malarial parasite triggered a strong inflammatory response, which in turn set off a powerful antibody response that cleared the parasite-infected cells. The intriguing thing is that malaria, chronic viral infections, and autoimmune diseases all share the same inflammatory signaling pathways, which suggests that this discovery could be exploited to improve treatment strategies for the latter as well.
The current study was led by researchers who have spent over ten years examining various aspects of the immune response to malaria. They cast some doubt on the long-held hypothesis that malarial infection is so successful because it manages to escape detection by the immune system, saying this is only one of its many adaptations to human parasitic existence.
Again, they point to the surprising lack of natural immunity following malarial infection. In most cases, protective immunity occurs after an infection with a bacterium or virus, lasting for life. However, says researcher Diana Hansen, “It is well known that an individual must continuously be exposed to malaria over many decades in order to develop protective immunity, during which time they are often sick, as well as spreading the disease.”
For further information please click here.
