Research Topic: Fungal immunology

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

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.

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

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.

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Protein kinase A signaling regulates immune evasion by shaving and concealing fungal β-1,3-glucan

Candida albicans, a common fungal pathogen, uses a clever strategy to hide from the immune system by masking a molecule on its surface that would normally trigger an immune response. Researchers used both computer modeling and laboratory experiments to show that this hiding strategy involves two main processes: the fungus grows and exposes the molecule, while simultaneously using enzymes to shave it away. They found that a cellular signaling pathway called PKA is essential for activating these shaving enzymes in response to lactate, a signal from the host environment.

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Immunomodulatory function of chitosan is dependent on complement receptor 3

This study reveals how the human immune system recognizes chitosan, a natural component found in the walls of disease-causing fungi like Aspergillus and Cryptococcus. Researchers discovered that immune cells use a protein called CR3 on their surface to detect and respond to chitosan by producing inflammatory chemicals that help fight infection. When chitosan works together with fungal proteins, it can boost the immune system’s response even more effectively, suggesting new ways to enhance immunity against fungal infections.

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Fungal vaccines: so needed, so feasible, and yet so far off

Fungal infections kill millions of people worldwide each year, particularly those with weakened immune systems, yet no vaccines exist to prevent them. Scientists have discovered that a specific fungal enzyme called Eng2 can trigger protective immune responses against three major disease-causing fungi. A vaccine containing this enzyme from all three fungi species could potentially protect against multiple dangerous fungal infections, though challenges like cost and the need to work in immunocompromised patients remain before such vaccines reach patients.

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

Scientists studied how the body’s immune system defends against Sporothrix brasiliensis, a dangerous fungus spreading through Latin America. They found that two immune receptors called dectin-1 and dectin-2 are crucial for fighting this infection by activating killer T cells and controlling regulatory T cells. Surprisingly, a cytokine called IL-17, commonly associated with fungal defense, actually helps maintain tissue integrity rather than directly killing the fungus.

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Ex Vivo Host Transcriptomics During Cryptococcus neoformans, Cryptococcus gattii, and Candida albicans Infection of Peripheral Blood Mononuclear Cells From South African Volunteers

Researchers studied how human immune cells respond to three different fungal infections that commonly affect people with weakened immune systems. By examining gene activity in blood cells exposed to these fungi, they discovered that each fungus triggers different immune responses, with Candida albicans causing a much stronger reaction than the two Cryptococcus species. Only one shared immune pathway was activated by all three fungi, suggesting each infection requires different immune mechanisms to fight off. These findings could help develop new treatments for serious fungal infections.

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Immunometabolic reprogramming in macrophages infected with active and dormant Cryptococcus neoformans: differential modulation of respiration, glycolysis, and fatty acid utilization

Researchers discovered that when fungal yeast cells enter a dormant state inside immune cells, they trigger different metabolic changes compared to actively growing yeast. While active yeast pushes immune cells to work harder metabolically, dormant yeast causes minimal stress but increases fat uptake by immune cells. This difference may explain how some fungal infections can remain hidden in the body for long periods without causing symptoms.

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