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* Cerrahpasa Medical Faculty, University of Istanbul, Istanbul, Turkey;
Laboratory of Investigational Dermatology, and
Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, NY 10021
Behçet’s disease (BD) is a multisystem inflammatory disorder of unknown etiology characterized by recurrent oral and genital ulcerations and uveitis, with varying other manifestations associated with vascular inflammation. A unifying feature of BD inflammation is the skin pathergy reaction (SPR), a nonspecific tissue hyperreactivity to minor trauma involving epithelial disruption. This study compared skin responses to needle prick in BD patients and normal healthy volunteers. Two study groups, each consisting of 10 BD patients with SPR+ and 6 controls, were evaluated using either immunohistochemistry or quantitative real-time PCR to measure inflammatory cell and cytokine levels in biopsy specimens obtained serially from independent sites at 0, 8, and 48 h after needle prick. We found similar cellular infiltration patterns in response to needle prick in BD patients and controls between 0 and 8 h. Further development of this immune response was limited in skin of normal control subjects, with stable or decreased inflammatory mediators observed at 48 h. In contrast, in BD-derived skin specimens, increased influxes of mature dendritic cells, monocytes, and lymphocytes, including T regulatory cells, were noted by 48 h. Similarly, increases in cytokines (IFN-
, IL-12 p40, IL-15), chemokines (MIP3-
, IP-10, Mig, and iTac), and adhesion molecules (ICAM-1, VCAM-1) were noted at 48 h in the skin of BD patients with SPR+ but not in the skin of normal controls. These results suggest that, in contrast to the self-limited inflammation associated with epithelial disruption of normal skin, BD patients experience marked cellular influxes into the injury site, leading to an exaggerated lymphoid Th1-type response.
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1 This work was supported by the Scientific & Technological Research Council of Turkey (to M.M.) and by the National Institutes of Health Grant K23-AR2187 (to S.O.).
2 Current address: Public Health Research Institute, Newark, NJ 07103.
3 Address correspondence and reprint requests to Dr. Stephen Oliver at the current address: Department of Medicine, New York University School of Medicine, New Bellevue 16N-1, 550 First Avenue, New York, NY 10016. E-mail address: olives03{at}med.nyu.edu
4 Abbreviations used in this paper: BD, Behçet’s disease; SPR, skin pathergy reaction; DC, dendritic cell; Tregs, T regulatory cell.
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