Allergic contact dermatitis.
Allergic contact dermatitis is a classic example of a cell mediated hypersensitivity reaction in the skin. This occurs as a result of xenobiotic chemicals penetrating into the skin, chemically reacting with self proteins, eventually resulting in a hapten-specific immune response. It is precisely because of this localized immune response that allergic signs and symptoms occur (redness, edema, warmth and pruritus). It has been known for years that conventional T-cells (CD4+ or CD8+ T-cells that express a T-cell receptor alpha/Beta) are critical effectors for this reaction. There is emerging evidence that innate immune lymphocytes such as invariant Natural killer T-cells and even Natural killer cells may play important role. Other T-cell types such as Tregulatory cells and the IL-10 secreting Tregulatory cells type I are likely to be important in the control (resolution) of allergic contact dermatitis. Other cell types that may contribute include B-cells and hapten-specific IgM. Additionally, epidermal Langerhans cells have been ascribed an indispensable role as an antigen presenting cell to educate T-cells of the skin immune system. Studies of mice that lack this cell type suggest that Langerhans cells may be dispensible, and may even play a regulatory role in allergic contact dermatitis. The identity of the antigen presenting cells that complement Langerhans cells has yet to be identified. Lastly, Keratinocytes play a role in all phases of allergic contact dermatitis, from the early initiation phase with the elaboration of inflammatory cytokines, that plays a role in Langerhans cell migration, and T-cell trafficking, through the height of the inflammatory phase with direct interactions with epidermotrophic T-cells, through the resolution phase of allergic contact dermatitis with the production of anti-inflammatory cytokines and tolerogenic antigen presentation to effector T-cells. As the understanding of allergic contact dermatitis continues to improve, this will provide novel therapeutic targets for immune modulating therapy.
Gober
Michael D
MD
University of Maryland School of Medicine, Baltimore, MD 21030, USA.
Gaspari
Anthony A
AA
D000818:Animals; D017951:Antigen Presentation; D015551:Autoimmunity; D001402:B-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D002465:Cell Movement / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D017449:Dermatitis, Allergic Contact / Q000276:immunology*; D006241:Haptens / Q000276:immunology; D006801:Humans; D007108:Immune Tolerance; D007113:Immunity, Innate; D007075:Immunoglobulin M / Q000276:immunology; D007249:Inflammation / Q000276:immunology; D007801:Langerhans Cells / Q000276:immunology*; D011948:Receptors, Antigen, T-Cell / Q000276:immunology; D012867:Skin / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D015262:Xenobiotics / Q000276:immunology
D016207:Cytokines; D006241:Haptens; D007075:Immunoglobulin M; D011948:Receptors, Antigen, T-Cell; D015262:Xenobiotics