Epidermal Langerhans cells have been implicated in the process by which animals skin painted with highly reactive haptens, such as DNFB, develop contact hypersensitivity. Compared to normal body wall skin, murine tail skin contains relatively few, unevenly distributed Langerhans cells; ultraviolet light exposure depletes the epidermis transiently of normal numbers of morphologically identifiable Langerhans cells. When mice are painted with DNFB on skin naturally or artificially depleted of Langerhans cells, contact hypersensitivity is not induced. More importantly, these animals become specifically unresponsive to the chemical contact, and are unable to mount effective hypersensitivity reactions if presented subsequently with an immunogenic regimen. It is concluded that Langerhans cells provide the skin with an intricate dendritic network just beneath the keratinized layer, the function of which is to receive, process and present cutaneously applied antigens in an immunogenic form. When this barrier network is breached, the host responds to antigenic exposure by becoming profoundly and specifically unresponsive. Implications of this hypothesis for epidermal virus infections and cutaneous malignancy are discussed.
|Original language||English (US)|
|Number of pages||4|
|Journal||Journal of Investigative Dermatology|
|Publication status||Published - 1980|
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