How Malaria Parasites escape From the Host’s Immune System

Malaria is among the most serious infectious diseases affecting people, representing around a large portion of a million deaths every year. Plasmodium falciparum causes most life-threatening cases of malaria. Obtained immunity to malaria is inefficient, even after repeated exposure to P. falciparum, however, the immune regulatory mechanisms utilized by P. falciparum remain to a large extent unknown.

Here we demonstrate that P. falciparum utilizes immune inhibitory receptors to achieve immune evasion. RIFIN proteins are products of a polymorphic multigene family comprising approximately 150– 200 genes for every parasite genome that are expressed on the surface of infected erythrocytes.

Scientists have found a molecular handshake’ that malaria fever parasites to escape from the host’s v. Researchers in Japan have found key molecules enabling malaria parasites to escape destruction by host immune cells.

They published their discoveries in Nature. Malaria is one of three major infectious diseases affecting approximately 300 million individuals consistently and representing around 500,000 deaths. To date, effective vaccines against malaria have not been effectively developed. Plasmodium falciparum causes particularly severe disease, among the malaria parasites infecting people.

Moreover, gained immunity to malaria is inefficient, even after repeated exposures to P. falciparum. The regulatory mechanisms utilized by P. falciparum to evade the immune system remain to a large extent unclear.

In this examination, a research group led by Professor Hisashi Arase at Osaka University found that proteins called RIFINs expressed on red platelets (erythrocytes) infected with P. falciparum help the parasite to suppress the host immune response, in this way resulting about severe malaria.

The RIFINs tie to a receptor called the LILRB1 which is found on the host’s immune cells—the B and natural killer cells. This elicits an immune inhibitory effect, whereby the host immune cells never again destroy the infected erythrocyte and its pathogenic payload.

The specialists additionally noticed that P. falciparum-contaminated erythrocytes isolated from patients with severe malaria will probably interact with LILRB1 than erythrocytes from patients with non-severe malaria.

This suggests the authoritative of RIFINS to LILRB1 is a key pathway in the pathogenesis of severe malaria. The outcomes of this research are expected upon to significantly add to the development of therapeutic medications and vaccines against malaria.

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