Journal
JOURNAL OF INVESTIGATIVE DERMATOLOGY
Volume 133, Issue 10, Pages 2311-2314Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/jid.2013.239
Keywords
-
Categories
Funding
- NCRR NIH HHS [UL1 RR024143, 5UL1RR024143-02] Funding Source: Medline
- NIGMS NIH HHS [GM07739, T32 GM007739] Funding Source: Medline
Ask authors/readers for more resources
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
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available