Journal
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 127, Issue 4, Pages 954-U196Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2010.12.1124
Keywords
Nonlesional; atopic dermatitis; altered terminal differentiation; immune activation
Categories
Funding
- National Center for Research Resources (NCRR) [5UL1RR024143-02]
- National Institutes of Health (NIH)
- NIH Roadmap for Medical Research
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Background: Atopic dermatitis (AD) is a common inflammatory skin disease with a TH2 and T22'' immune polarity. Despite recent data showing a genetic predisposition to epidermal barrier defects in some patients, a fundamental debate still exists regarding the role of barrier abnormalities versus immune responses in initiating the disease. An extensive study of nonlesional AD (ANL) skin is necessary to explore whether there is an intrinsic predisposition to barrier abnormalities, background immune activation, or both in patients with AD. Objective: We sought to characterize ANL skin by determining whether epidermal differentiation and immune abnormalities that characterize lesional AD (AL) skin are also reflected in ANL skin. Methods: We performed genomic and histologic profiling of both ANL and AL skin lesions (n = 12 each) compared with normal human skin (n = 10). Results: We found that ANL skin is clearly distinct from normal skin with respect to terminal differentiation and some immune abnormalities and that it has a cutaneous expansion of T cells. We also showed that ANL skin has a variable immune phenotype, which is largely determined by disease extent and severity. Whereas broad terminal differentiation abnormalities were largely similar between involved and uninvolved AD skin, perhaps accounting for the background skin phenotype,'' increased expression of immune-related genes was among the most obvious differences between AL and ANL skin, potentially reflecting the clinical disease phenotype.'' Conclusion: Our study implies that systemic immune activation might play a role in alteration of the normal epidermal phenotype, as suggested by the high correlation in expression of immune genes in ANL skin with the disease severity index. (J Allergy Clin Immunol 2011;127:954-64.)
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