T cell immunotherapies trigger neutrophil activation to eliminate tumor antigen escape variants. T cell immunotherapies trigger neutrophil activation to eliminate tumor antigen escape variants
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This SuperSeries is composed of the SubSeries listed below. Overall design: Refer to individual Series
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2023-02-06
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This study describes the target receptor and mechanism of action of Staphylococcal superantigen like 13 (SSL13), a secret protein reside on S.aureus immune evasion cluster 2(IEC-2) that previously supposed to modulate immune evasion. In sharp contrast to the characterized SSLs located on the staphylococcal pathogenicity island 2 (SPI-2) , that inhibit immune functions, We demonstrate SSL13 is a chemoattractant and a neutrophil activator that acts via the FPR2. Therefore, SSL13 is a unique SSL member not belonging to the immune evasion class, but is a pathogen alarming molecule sensed by the FPR2. Our study provides a new conception of SSLs, that not only inhibit host immune processes but also recruit human neutrophils to the site of infection, where S. aureus can be disarmed by secreted immune evasion proteins and used as vesicles to other parts of the host. This allow us to better understand of S. aureus pathological processes.. SSL13 activates neutrophils via FPR2
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