Observations about the body’s response to malaria infection can lead to new treatments for HIV and lupus, investigators believe.
Thanks to a discovery about the immune system’s response to malaria, better treatments for HIV and lupus may be on the horizon, according to a new paper published Cell Reports. This can be accomplished either through new therapies or yet-to-be-developed vaccines.
Investigators from Australia continued their work examining the relationship between the host immune system and malaria infection. It was previously assumed that the infection avoids detection within the immune system—a major reason for our inability to fight malaria.
“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,” study author Diana Hansen, BMedSc, PhD, said in a press release. The team wanted to examine what made malaria different than other diseases because in most cases, a single exposure can result in lifelong immunity.
At the outset of the study, the study authors anticipated that inflammation would negatively impact B cells. The team was building on a previous study of theirs which demonstrated how inflammatory signals activated molecules that inhibited the development of T cells. That meant that B cells were unable to learn to make antibodies.
However, the investigators learned that inflammatory signals improved the quality of antibodies being produced. Malaria had not been previously known to cause the body to produce potent antibodies, but that’s what the investigators observed. They called it “elite training” where antibodies learned to become “professional predators.”
“What we determined was that inflammatory signals simultaneously improve the quality of the antibody response, while limiting its magnitude,” Hansen continued. “The B cells, even though they are of elite quality, are not able to have as much impact on future infections.”
Malaria, HIV, and chronic hepatitis C are similar in that high quality and potent antibodies are required for the body to fight off the infections.
“We have identified the molecular ‘switch’ that drives the immune system to produce highly potent antibodies, and the inflammatory signals that influence its function,” Hansen said, explaining that when these high quality and potent antibodies target self-antigens, it results in autoimmune diseases such as lupus. “Targeting this molecule, or other molecules in the same pathway, could offer a more ‘precision medicine’ approach to treating these diseases than currently exists.”
The opportunity these findings offer are vast and could impact a variety of chronic viral infections and autoimmune diseases, the investigators said. Eventually, they hope to create vaccines or therapies that would “switch on” the molecules which produce these elite B cells to better fight these infections.
Conversely, the study authors said, vaccines or therapies could “switch off” the autoimmune disease trigger molecules to inhibit the production of B cells, like in the case with lupus.
As the investigators offer more of an insight into how these antibodies operate, the hope is that they will eventually be able to change the way it functions in response to chronic infections.