S100a4 mediated peritoneal B1 lymphocytes play a critical role in host protection against helminth infection.

BACKGROUND

Trichinellosis is a globally prevalent parasitic disease caused by infection of Trichinella spiralis. B1 cells are critically involved in immune defense against multiple parasitic infections, yet their functional role in trichinellosis remains uncharacterized.

METHODS

Wild-type, Btk conditional knockout and S100a4 knockout mice were used to construct the infection model of T. spiralis. The proportions and BCR signaling of peritoneal B1 cells in mice infected with T. spiralis were detected with flow cytometry and immunofluorescence. RNA sequencing was applied to analyze the possible mechanisms of B1 cell activation. ELISA was used to detect the production of antibodies.

RESULTS

Peritoneal B1 cells exhibited obvious accumulation with enhanced B cell receptor (BCR) signaling at the muscle phase of murine T. spiralis infection. B1 cell deficiency impaired host immune responses against T. spiralis at the muscle stage, confirming the essential contribution of B1 cells to anti-trichinella immunity. RNA sequencing analysis revealed significant upregulation of S100A4 in peritoneal B1 cells following infection. Mechanistically, S100A4 regulated the biological functions of peritoneal B1 cells through modifying cell relocation, BCR signaling, and antibody production.

CONCLUSIONS

Our findings reveal a previously unrecognized role of S100A4-mediated B1 cell responses in host defense against T. spiralis infection. The data provide new mechanistic insights into the immune regulation of trichinellosis.