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

Summary

Scientists studied how the immune system fights a dangerous fungal infection called sporotrichosis caused by Sporothrix brasiliensis. They found that two immune receptors called dectin-1 and dectin-2 are crucial for fighting this infection by activating specific killer T cells and preventing immune suppression. Unlike what was previously thought, these receptors don’t work mainly by triggering inflammation, but rather by fine-tuning the balance of different immune cell types. This discovery could help develop new treatments for this emerging fungal disease.

Background

Sporothrix brasiliensis is an emerging fungal pathogen responsible for epidemic outbreaks of sporotrichosis in Latin America, characterized by higher aggressiveness and zoonotic transmission. The C-type lectin receptors dectin-1 and dectin-2 play key roles in antifungal immunity, but their specific contribution against S. brasiliensis has not been fully characterized.

Objective

To determine the contribution of dectin-1 and dectin-2 receptors to host protection against S. brasiliensis in a murine model of disseminated sporotrichosis and to identify the immunological mechanisms underlying their protective effects.

Results

Dectin-1 and dectin-2 were essential for host survival and limiting fungal dissemination. Their protective effects were mediated primarily by shaping T cell responses, particularly by promoting cytotoxic CD8+ T cells and limiting regulatory T cells, rather than through conventional TH17 responses. IL-17 contributed to host survival but not to direct fungal restriction.

Conclusion

Dectin-1 and dectin-2 are critical determinants of protection against S. brasiliensis through mechanisms involving balance of CD8+ T cells and Tregs rather than IL-17-dependent responses, expanding understanding of sporotrichosis pathophysiology and identifying potential therapeutic targets.
  • Published in:Frontiers in Immunology,
  • Study Type:Experimental Animal Study,
  • Source: PMC12507893, PMID: 41080603, DOI: 10.3389/fimmu.2025.1668445
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