Is/are pattern recognition receptor(s) for Staphylococcus aureus defective in atopic dermatitis?
It is known that Staphylococcus aureus induces the expression of human beta-defensin-2 (hBD-2), a well-characterized antimicrobial peptide, in keratinocytes. However, in spite of heavy colonization of atopic dermatitis (AD) skin lesions by S. aureus, these lesions have consistently been shown to contain low expression of hBD-2. The current article discusses various possible mechanisms for the low expression of hBD-2 in AD and raises the question whether the innate recognition of S. aureus by keratinocytes in AD is intact.
Ong
Peck Y
PY
Division of Clinical Immunology/Allergy, Department of Pediatrics, Childrens Hospital Los Angeles/Keck School of Medicine, University of Southern California, Los Angeles, CA 90027, USA. pyong@chla.usc.edu
D003876:Dermatitis, Atopic / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology; D006801:Humans; D015603:Keratinocytes / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D051192:Receptors, Pattern Recognition / Q000276:immunology; D013203:Staphylococcal Infections / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology; D013211:Staphylococcus aureus / Q000276:immunology*; D051193:Toll-Like Receptors / Q000276:immunology; D023083:beta-Defensins / Q000276:immunology / Q000378:metabolism*
C106641:DEFB4A protein, human; D051192:Receptors, Pattern Recognition; D051193:Toll-Like Receptors; D023083:beta-Defensins