# Plasmodium yoelii surface-related antigen (PySRA) modulates the host pro-inflammatory responses via binding to CD68 on macrophage membrane

## TL;DR

A protein from the malaria parasite binds to a macrophage receptor, modulating inflammation and offering potential for new treatments.

## Contribution

Discovery that PySRA-F2 modulates inflammation via CD68 binding and its protective effect in mice.

## Key findings

- PySRA-F2 activates MAPK and NF-κB pathways by binding to CD68 on macrophages.
- Anti-PySRA-F2 antibody protects mice from P. yoelii infection.
- Inflammatory responses like IL-1β, TNF-α, and IL-6 are reduced with PySRA-F2.

## Abstract

Malaria, one of the major infectious diseases in the world, is caused by the Plasmodium parasite. Plasmodium antigens could modulate the inflammatory response by binding to macrophage membrane receptors. As an export protein on the infected erythrocyte membrane, Plasmodium surface-related antigen (SRA) participates in the erythrocyte invasion and regulates the immune response of the host. This study found that the F2 segment of P. yoelii SRA activated downstream MAPK and NF-κB signaling pathways by binding to CD68 on the surface of the macrophage membrane and regulating the inflammatory response. The anti-PySRA-F2 antibody can protect mice against P. yoelii, and the pro-inflammatory responses such as IL-1β, TNF-α, and IL-6 after infection with P. yoelii are attenuated. These findings will be helpful for understanding the involvement of the pathogenic mechanism of malaria with the exported protein SRA.