The innate immune system evolved more than 2 billion years ago to first recognize
pathogens then eradicate them. Several distinct defects in this ancient but rapidly responsive
element of human immune defense account for the increased incidence of skin
infections in atopics. These defects include abnormalities in the physical barrier of the
epidermis, alterations in microbial pattern recognition receptors such as toll receptors and
nucleotide binding oligomerization domains, and a diminished capacity to increase the
expression of antimicrobial peptides during inflammation. Several antimicrobial peptides
are affected including; cathelicidin, HBD-2, and HBD-3, which are lower in lesional skin of
atopics compared with other inflammatory skin diseases, and dermcidin, which is decreased
in sweat. Other defects in the immune defense barrier of atopics include a relative
deficiency in plasmacytoid dendritic cells. In the future, understanding the cause of these
defects may allow therapeutic intervention to reduce the incidence of infection in atopic
individuals and potentially decrease the severity of this disorder.
Semin Cutan Med Surg 27:144-150 © 2008 Elsevier Inc. All rights reserved.