Abstract
Contact hypersensitivity (CHS) is a prototype of delayed-type hypersensitivity (DTH) reactions. Since the initial observation that lymphocytes are in close apposition to Langerhans cells (LCs) during CHS, there is a great deal of evidence that supports the role of LCs in afferent and efferent limbs of CHS. Recent studies indicate that LCs mature into potent antigen-presenting cells (APCs) by upregulating their expression of a variety of molecules that facilitate their interaction with type 1 T-helper cells (TH1). Such THis are thought to produce a pattern of lymphokines that mediates the inflammatory response in CHS reactions. It is now recognized that keratinocytes (KCs) also play an important role in CHS. By producing a variety of proinflammatory cytokines, KCs have the ability to activate LCs, co-stimulate T-cell proliferative responses, and recruit mast cells during CHS reactions. KCs also produce immunosuppressive cytokines that may dampen CHS reactions. Lastly, immune-associated antigen (la+)KCs are tolerogenic APCs that may play an important role in terminating CHS by inducing clonal anergy (immunologic unresponsiveness) in TH1. If this mechanism is defeated, this may result in chronic CHS reactions. These advances in our understanding of CHS further support the concept that the skin, particularly the epidermis, is a dynamic, immunologic organ capable of initiating, amplifying, and terminating hypersensitivity reactions in this most peripheral “outpost” of the immune system.
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