Wellcome Senior Fellow Associate Professor Gordon Brown and his group have published research in the Nature Immunology journal (January 2007) showing how Dectin-1, a cell-surface protein, protects the body from common fungal infections like Candida and Aspergillus.
"This is a major advancement in our understanding of how the immune system recognises and responds to fungal infections," said Brown, based at UCT's Institute for Infectious Disease and Molecular Medicine.
Fungal infections are more common today than ever before, a result of compromised immune systems. Those with advanced HIV are also particularly susceptible to fungal infections.
Brown's main interest lies in identifying and characterising the surface molecules (receptors) on immune cells that recognise pathogens. The Dectin-1 protein, for example, plays an important role in recognising the presence of pathogenic fungi.
"In the Nature Immunology paper, we have generated a mouse in which the gene encoding Dectin-1 had been deleted. Dectin-1 is a receptor we identified in 2001 and have shown over the past few years to be capable of mediating the recognition and response to fungal pathogens."
They describe how the deletion of Dectin-1 in mice results in heightened susceptibility to fungal infection.
The two independent groups cited in the January issue, one led by Brown and the other by Yoichiro Iwakura at the University of Tokyo, also evaluated the types of blunted immune responses that occur in the mutant mice and showed that only specific anti-fungal immune functions become defective.
"These studies substantially extend our understanding of how pathogenic fungi affect host tissues and the requirement of Dectin-1 in those processes."
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