Where it comes from
- Made in
- Keratinocytes, tonsil, airway, gingiva and placenta, induced by injury and infection
- Sent out by
- Wounding, bacteria and interferon-gamma switch it on
- Acts on
- Staphylococcus aureus including MRSA
- Streptococci
- Candida
- HIV
What it does
- Kills Gram-positive bacteria at physiological salt, which most defensins cannot
- Blocks lipid II, the cell-wall building block, as vancomycin does
- Binds the melanocortin receptor MC1R, which in dogs sets coat colour
In medicine
Beyond the body’s own use
- It blocks lipid II, the cell-wall building block vancomycin binds, so it is studied as a template for antibiotics against resistant Gram-positive bacteria 2
- Engineered versions are tested on skin and implant infections in animals; none has reached a human trial
- The dog version of this gene sets black coat colour through the melanocortin receptor, the clearest evidence that a defensin can double as a pigment signal 3
Sources
- Harder et al., Isolation and characterization of human beta-defensin-3, Journal of Biological Chemistry 2001
- Sass et al., Human beta-defensin 3 inhibits cell wall biosynthesis in staphylococci, Infection and Immunity 2010
- Candille et al., A beta-defensin mutation causes black coat colour in domestic dogs, Science 2007
- Hollox et al., Psoriasis is associated with increased beta-defensin genomic copy number, Nature Genetics 2008
This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.