Anti-Therapeutic Action: β-1

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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Kre6-dependent β-1,6-glucan biosynthesis only occurs in the conidium of Aspergillus fumigatus

Researchers discovered that a specific sugar compound called β-1,6-glucan is found in the spore-like reproductive structures (conidia) of the fungus Aspergillus fumigatus but not in its growing filaments (mycelium). Using advanced nuclear magnetic resonance technology, they identified the KRE6 gene as responsible for making this sugar and found that removing this gene makes the fungus more vulnerable to certain chemicals that damage fungal cell walls.

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

Candida albicans is a fungus that causes infections in humans. The fungus has developed a clever way to hide from our immune system by covering up a molecule on its surface called β-1,3-glucan that normally triggers immune responses. This study shows that the fungus masks this molecule through a combination of growing and dividing to create new surfaces, and then using enzymes to trim away exposed molecules. The research reveals that a specific cell signaling pathway controlled by lactate (a chemical found in our bodies) activates this masking behavior, helping the fungus evade immune recognition.

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