A type of white blood cells called neutrophils combines with helper T cells to create inflammation due to skin contact with allergen, a group of scientists led by Raif Geha at Harvard Medical School has shown in a mouse model of eczema.
The researchers showed that by blocking the neutrophils' ability to produce a signaling molecule called leukotriene B4 (LTB4), they could prevent the accumulation of both neutrophils and T cells, and hence inflammation, in skin that had been mildly irritated and exposed to a model antigen.
The research was published in the journal Immunity. [paper] [media summary]
The scientists were investigating the role of neutrophils, which are attracted to the site of scratching. They suggest that blocking LTB4's interaction with its receptor (not necessarily by the drug they used, bestatin) could prevent sudden eczema flares in patients that were exposed to something they were allergic to.
The research doesn't sound immediately useful to me, as the real problem with eczema--or atopic dermatitis--is that in general we don't know the cause, and flares aren't usually triggered by direct exposure to something you're allergic to. But it is interesting to learn that neutrophils are flooding scratched skin, and that they are recruiting other neutrophils and T cells--I would like to see whether a drug reducing this phenomenon might calm down itch. As always, the details are in the drug discovery process: finding something that works, isn't toxic and doesn't have weird side effects.