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‘Self-sabotage’ prevents immune protection

December 29
02:17 2015
Australian scientists have for the first time revealed how malaria parasites cause an inflammatory reaction that sabotages our body's ability to protect itself against the disease.Dr. Axel Kallies (left) and Dr. Diana Hansen (right) from Melbourne's Walter and Eliza Hall Institute said the discovery opens up the possibility of improving new or existing malaria vaccines by boosting key immune cells needed for long-lasting immunity.

Australian scientists have for the first time revealed how malaria parasites cause an inflammatory reaction that sabotages our body’s ability to protect itself against the disease.Dr. Axel Kallies (left) and Dr. Diana Hansen (right) from Melbourne’s Walter and Eliza Hall Institute said the discovery opens up the possibility of improving new or existing malaria vaccines by boosting key immune cells needed for long-lasting immunity.

MELBOURNE: Malaria parasites cause an inflammatory reaction that sabotages our body’s ability to protect itself against the deadly disease, scientists have found for the first time.

The finding opens up the possibility of improving malaria vaccines by boosting key immune cells needed for long-lasting immunity. This could even include vaccines that have previously been ineffective in clinical trials.

Researchers found 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.

Diana Hansen, Axel Kallies and Victoria Ryg-Cornejo led a research team from Walter and Eliza Hall Institute in Australia that examined how the immune system responded to malaria infection caused by Plasmodium falciparum.

Hansen said it is the first time scientists have pinpointed why the immune system fails to develop immunity during malaria infection.

“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,” Ms. Hansen said.

“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 reinfection and become sick many times, as well as spreading the disease,” she said.

Mr. Kallies said inflammatory molecules released by the body to fight the infection prevent protective antibodies from being made.

“Specialized immune cells called helper T cells join forces with B cells to generate these protective antibodies,” Mr. Kallies said.

“However, we showed that 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.

Malaria is one of the most serious human infectious diseases, with about 250 million clinical cases each year.

Children are particularly susceptible to severe malaria because they have little or no immunity to the parasite.

Severe malaria causes symptoms including anaemia, breathing difficulties, kidney failure and coma, and can quickly lead to death.

Hansen said the findings could lead to new avenues in the search for effective malaria vaccines.
“This research opens the door to therapeutic approaches to accelerate development of protective immunity to malaria and improve efficacy of malaria vaccines,” Ms. Hansen said.

“Until now, malaria vaccines have had disappointing results. We can now see a way of improving these responses, by tailoring or augmenting the vaccine to boost development of helper T cells that will enable the body to make protective antibodies that target the malaria parasites,” she said.
The study was published in the journal Cell Reports. -PTI

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