Allergic and immunologic skin disorders.

The skin represents a unique immunologic organ poised to protect the host from invading organisms and environmental antigens. The skin is also an important target for a variety of allergic and autoimmune responses. Mast cells are key to the pathogenesis of urticaria, angioedema, and mastocytosis. Atopic dermatitis is the consequence of an immunoregulatory abnormality resulting in a skin-directed T helper type 2 response. Allergic contact dermatitis is an example of classic delayed type hypersensitivity. Circulating autoantibodies against the epidermis are a key mechanism by which bullous skin diseases occur.

[1]  V. Deleo,et al.  Contact and Occupational Dermatology , 1997 .

[2]  E. Charlesworth,et al.  Urticaria and angioedema: a clinical spectrum. , 1996, Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology.

[3]  J. Marks.  North American Contact Dermatitis Group standard tray patch test results (1992 to 1994) , 1996 .

[4]  J. Katz,et al.  Resolution of chronic urticaria in patients with thyroid autoimmunity. , 1995, The Journal of allergy and clinical immunology.

[5]  D. Leung,et al.  Atopic dermatitis: the skin as a window into the pathogenesis of chronic allergic diseases. , 1995, The Journal of allergy and clinical immunology.

[6]  L. Picker,et al.  Milk-induced eczema is associated with the expansion of T cells expressing cutaneous lymphocyte antigen. , 1995, The Journal of clinical investigation.

[7]  P. Cruz.  What accounts for contact allergy , 1994 .

[8]  V. Aoki,et al.  Brazilian pemphigus foliaceus, endemic pemphigus foliaceus, or fogo selvagem (wild fire). , 1994, Dermatologic clinics.

[9]  F. Simons,et al.  The pharmacology and use of H1-receptor-antagonist drugs. , 1994, The New England journal of medicine.

[10]  J. Troy,et al.  A passive transfer model of the organ-specific autoimmune disease, bullous pemphigoid, using antibodies generated against the hemidesmosomal antigen, BP180. , 1993, The Journal of clinical investigation.

[11]  H. Sampson,et al.  Presence of IgE antibodies to staphylococcal exotoxins on the skin of patients with atopic dermatitis. Evidence for a new group of allergens. , 1993, The Journal of clinical investigation.

[12]  J. Zone,et al.  Dermatitis herpetiformis and linear IgA bullous dermatosis. , 1993, Dermatologic clinics.

[13]  R. Briggaman,et al.  Epidermolysis bullosa acquisita and bullous systemic lupus erythematosus. Diseases of autoimmunity to type VII collagen. , 1993, Dermatologic clinics.

[14]  J. Kochan,et al.  Autoantibodies against the high-affinity IgE receptor as a cause of histamine release in chronic urticaria. , 1993, The New England journal of medicine.

[15]  D. Williams,et al.  Altered metabolism of mast-cell growth factor (c-kit ligand) in cutaneous mastocytosis. , 1993, The New England journal of medicine.

[16]  N. Pelc,et al.  Paraneoplastic Pemphigus: An Autoimmune Mucocutaneous Disease Associated with Neoplasia , 1990 .

[17]  H. Sampson,et al.  The role of allergens in atopic dermatitis. , 1993, Clinical reviews in allergy.

[18]  C. Hauser,et al.  The role of microorganisms in atopic dermatitis. , 1993, Clinical reviews in allergy.

[19]  N. Soter.  The skin in mastocytosis. , 1991, The Journal of investigative dermatology.

[20]  R. Freeman,et al.  Herpes gestationis: clinical and histologic features of twenty-eight cases. , 1983, Journal of the American Academy of Dermatology.

[21]  G. Rajka,et al.  Diagnostic Features of Atopic Dermatitis , 1980, Acta Dermato-Venereologica.