Where it comes from
- Made in
- Neutrophils, which store it in their azurophilic granules; some in natural killer and T cells and in monocytes
- Sent out by
- When the neutrophil swallows a microbe or dies at a site of infection
- Acts on
- Bacteria, fungi and enveloped viruses
- Immune cells (chemotaxis)
- Host cells at high concentration
What it does
- Kills microbes inside the phagosome
- Blocks bacterial toxins (anthrax lethal factor, diphtheria toxin) by binding them
- Attracts T cells and immature dendritic cells
- Toxic to the body’s own cells at high levels, as in inflamed lungs
In medicine
- Measured in research as a marker of neutrophil activation; high in the sputum of cystic fibrosis and in sepsis
- No medicine. Its gene sits in a tandem array of four to eleven copies per person, and the proportions of HNP-1 and HNP-3 follow the copies 3
Beyond the body’s own use
- Defensins inspired many antimicrobial peptide drugs; none built on HNP-1 has reached approval
- It binds and neutralises anthrax lethal toxin, and protected mice against a lethal dose of it, which is studied as a way to blunt toxin-driven disease 2
- Copy number of the gene array is studied as a risk factor in infection; what it does to the total amount of defensin a person makes is not settled 3
Sources
- Ganz et al., Defensins: natural peptide antibiotics of human neutrophils, Journal of Clinical Investigation 1985
- Kim et al., Human alpha-defensins neutralize anthrax lethal toxin, Proceedings of the National Academy of Sciences 2005
- Aldred et al., Copy number polymorphism of the alpha-defensin genes DEFA1 and DEFA3, Human Molecular Genetics 2005
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.