title: Mechanisms of contact sensitization offer insights into the role of barrier defects vs. intrinsic immune abnormalities as drivers of atopic dermatitis.
abstract: Atopic dermatitis (AD) is a common inflammatory skin disease characterized by wet, oozing, erythematous, pruritic lesions in the acute stage and xerotic, lichenified plaques in the chronic stage. It frequently coexists with asthma and allergic rhinitis, sharing some mechanistic features with these diseases as part of the "atopic march." Controversy exists as to whether immune abnormalities, epidermal barrier defects, or both are the primary factors responsible for disease pathogenesis. In AD patients, there is often a coexisting irritant contact dermatitis (ICD) or allergic contact dermatitis (ACD) that is sometimes clinically difficult to distinguish from AD. ACD shares molecular mechanisms with AD, including increased cellular infiltrates and cytokine activation (Gittler et al., 2013). In this issue, Newell et al. (2013) used an experimental contact sensitization model with dinitrochlorobenzene (DNCB) to gain insight into the unique immune phenotype of AD patients.
authors.affiliation: Laboratory for Investigative Dermatology, The Rockefeller University, New York, New York, USA; Columbia University College of Physicians and Surgeons, New York, New York, USA.
authors.forename: Nikhil
authors.initials: N
authors.lastname: Dhingra
authors.affiliation: Laboratory for Investigative Dermatology, The Rockefeller University, New York, New York, USA.
authors.forename: Nicholas
authors.initials: N
authors.lastname: Gulati
authors.affiliation: Laboratory for Investigative Dermatology, The Rockefeller University, New York, New York, USA; Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, New York, USA. Electronic address: Emma.Guttman@mountsinai.org.
authors.forename: Emma
authors.initials: E
authors.lastname: Guttman-Yassky
mesh_terms: D017449:Dermatitis, Allergic Contact / Q000276:immunology*; D003876:Dermatitis, Atopic / Q000276:immunology*; D005260:Female; D006801:Humans; D008297:Male; D012867:Skin / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*
references.citation: J Allergy Clin Immunol. 2011 Apr;127(4):954-64.e1-4
references.pmid: 21388663
references.citation: J Allergy Clin Immunol. 2011 Jun;127(6):1420-32
references.pmid: 21419481
references.citation: J Invest Dermatol. 2007 Jun;127(6):1430-5
references.pmid: 17273160
references.citation: Proc Natl Acad Sci U S A. 2007 Mar 27;104(13):5557-62
references.pmid: 17372219
references.citation: J Allergy Clin Immunol. 2013 Feb;131(2):300-13
references.pmid: 22939651
references.citation: N Engl J Med. 2011 Oct 6;365(14):1315-27
references.pmid: 21991953
references.citation: J Invest Dermatol. 2013 Oct;133(10):2372-2380
references.pmid: 23528819
references.citation: J Allergy Clin Immunol. 2011 Sep;128(3):574-82.e1-12
references.pmid: 21704361