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Dectin-1 and dectin-2 drive protection against Sporothrix brasiliensis in experimental sporotrichosis

Summary

Researchers studied how the body fights a dangerous fungus called Sporothrix brasiliensis that causes sporotrichosis. They found that two immune receptors called dectin-1 and dectin-2 are crucial for protecting against this infection in mice. Surprisingly, these receptors work by activating killer immune cells and controlling regulatory immune cells, rather than through the typical immune response pathway scientists expected.

Background

Sporothrix brasiliensis is an emerging fungal pathogen causing epidemic sporotrichosis in Latin America with higher aggressiveness and zoonotic transmission. C-type lectin receptors dectin-1 and dectin-2 are key sensors in fungal recognition and antifungal immunity. The immunological markers of protection against S. brasiliensis are not fully characterized.

Objective

To uncover the contribution of dectin-1 and dectin-2 against S. brasiliensis in a murine model of disseminated sporotrichosis and identify the immunological mechanisms of protection.

Results

Dectin-1 and dectin-2 were essential for host survival and limiting fungal dissemination. Protection was mediated through shaping cytotoxic CD8+ and regulatory T cell populations rather than conventional TH17 responses. IL-17 contributed to survival but not fungal restriction.

Conclusion

Dectin-1 and dectin-2 are novel determinants of protection against S. brasiliensis, but their effector function involves balancing immunosuppressive responses rather than inducing IL-17-dependent antifungal immunity, expanding understanding of sporotrichosis pathophysiology.
  • Published in:Frontiers in Immunology,
  • Study Type:Experimental Animal Study,
  • Source: PMID: 41080603, DOI: 10.3389/fimmu.2025.1668445
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