Stress and the skin: a meeting report of the Weill Cornell Symposium on the Science of Dermatology.

Experts from around the world gathered for the Weill Cornell Symposium on the Science of Dermatology,* which explored the physiological manifestations of stress and its effects on skin, with three days of presentations and two poster sessions. Organized and introduced by Richard D. Granstein of the Weill Medical College of Cornell University (New York, NY), the conference began with discussions of the neuroanatomy of skin and mechanisms of cutaneous immunity and moved on to presentations on the modulation of cutaneous immunity by stress. Subsequently, presentations on stress effects on skin barrier function and wound healing were given. The conference concluded with discussions regarding the role of stress in several cutaneous diseases, including acne, psoriasis, atopic dermatitis, urticaria, hair disorders, and cancer. Some of the themes of the meeting are reported here; the abstracts from the meeting were published in the July issue (J Invest Dermatol 126:1665–81, 2006). In the keynote presentation, Esther M. Sternberg of the National Institutes of Health (Bethesda, MD) discussed the definition of stress and mechanisms through which its effects are mediated, focusing on her work regarding the hypothalamic–pituitary axis. Overactivation of this axis, as occurs in chronic stress, leads to a state of relative immunosuppression related to the effects of glucocorticoids. A blunted hypothalamic–pituitary axis, however, has been associated with autoimmune and inflammatory disease, including systemic lupus erythematosus and atopic skin disease. Similarly, tissue resistance to glucocorticoids — resulting from abnormal glucocorticoid receptor function — is associated with autoimmune disease. That bacterial toxins can repress glucocorticoid receptors suggests new potential mechanisms from which these inflammatory aberrations might result. Dieter Metze of the University of Munster (Germany) presented a view of the neuroanatomy of skin, where the close contact of neural structures with various immune cells is one basis for an interaction of the nervous and cutaneous immune systems. Kevin D. Cooper of Case Western Reserve University (Cleveland, OH) discussed the extraordinary scope of this skin immune system, where multiple inputs into skin control of inflammation are derived from the neurocutaneous axis, creating a pathway for stress to modulate cutaneous immunity. Richard D. Granstein of the Weill Medical College of Cornell University (New York, NY) presented evidence that nerve-derived factors regulate antigen presentation by Langerhans cells in skin. Langerhans cells have been found to express receptors for several neuropeptides as well as adrenergic receptors, and exposure to some of these mediators leads to inhibition of antigen presentation and modification of cytokine expression. Doina Ganea of Temple University School of Medicine (Philadelphia, PA) provided further evidence of the potentially antiinflammatory role of certain neuropeptides, demonstrating that vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) contribute to the development of bone marrow-derived tolerogenic dendritic cells in vitro and in vivo. Other topics addressed in this section included the regulatory role of melanocortins in skin (Thomas Luger, University of Munster, Germany), the role of stress in mediating peripheral sensitization of nerve fibers (thereby affecting perception of pain and itch) (Sonja Stander, University of Munster, Germany), the role of epidermal keratinocytes in cutaneous immune responses, and the effects of corticotropin-releasing hormone on mast cell-dependent vascular permeability (Theoharis C. Theoharides, Tufts University, Boston, MA). Melanie Flint (University of Pittsburgh, PA) discussed fascinating effects of restraint stress in mice on gene expression in T cells, indicating that stress activates genes responsible for priming the T cell to undergo either apoptosis or proliferation. Firdaus S. Dhabar of Stanford University (Stanford, CA) discussed the complex effects of stress on immunity and implications for cutaneous malignancies. Whereas acute stress can be immunoenhancing, chronic stress is generally immunosuppressive and increases susceptibility to skin cancer via suppression of T-helper 1-type cytokines, among other mechanisms. Ronald Glaser (Ohio State University, Columbus, OH) gave an overview of stress-induced immune dysfunction with a discussion of possible effects on cancer, heart disease, diabetes, wound healing, and the response to vaccination. George Maestroni (Cantonal Institute of Pathology, Locarno, Switzerland) discussed the regulatory role of catecholamines in cutaneous immu-