Current advances

Exposure to ultraviolet radiation can lead to both local and systemic immunologic defects. In particular, Langerhans cell depletion and dysfunction play a central role in ultraviolet light-induced immunosuppression. Ultraviolet light B (wavelength 290-320 nm) can induce Langerhans cell phenotypic changes and death; it also leads to the repopulation of epidermis with CD36+ macrophage-likc dendritic cells 24-72 h after exposure. Functionally, the lack of normal Langerhans cells and the presence of abnormal Langerhans cells and macrophage-like cells leads to impaired contact sensitivity. Specifically, application of a contact allergen to ultraviolet light B-irradiated skin can induce tolerance for that particular antigen. In addition, it has been proposed that mice and humans susceptible to the development of skin cancer are those susceptible to ultraviolet light B-induced defects in contact sensitization. These studies suggest that short-term immunologic defects induced by ultraviolet light are linked to long-term defects in processing and presentation of tumor antigens. Thus, in addition to foreign antigen recognition, Langerhans cells are probably important in tumor surveillance within skin.

Epidermal Langerhans cells can be targets for HIV

infection both in vitro and in vivo, however, most studies show that they do not represent a major reservoir for virus. In contrast, Langerhans cells in genital mucosa (where no stratum corneum exists) may be more easily infected by HIV and therefore may be the first cells infected during initial sexual exposure to HIV. Following emigration to regional lymph nodes, HIV-exposed Langerhans cells may then transmit virus to CD4f T cells. In support of this theory, Langerhans cells and other dendritic cells pulsed with HIV in vitro transmit high levels of infection to co-cultured T cells. Interestingly, this efficient transmission of virus does not require dendritic cell infection to occur per se. That is, these cells can capture HIV within their prominent cell surface den dritic processes in an infection-independent manner; subsequently, captured virus is transmitted to T cells during the process of antigen-specific T cell activation. Additionally, impaired Langerhans cell function has been proposed as an important factor in the pathogenesis of HIV-associated skin diseases, although initial studies to assess the function of Langerhans cells isolated from skin of HIV-infected individuals failed to detect marked defects in antigen presentation.

See also: Acquired immune deficiency syndrome

(AIDS); Antigen presentation via MHC class I molecules; Antigen presentation via MHC class II molecules; CD1; Contact hypersensitivity; Cytokines; Dendritic cells; Photoimmunology; Skin, contribution to immunity.

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