Important note: Information in this article was accurate in 1995. The state of the art may have changed since the publication date.
Cutaneous immunosurveillance and its role in skin cancer (Meeting abstract).
Melanoma Res; 3:4 1993. Unique Identifier : AIDSLINE ICDB/95607226 Stingl G; Department of Dermatology, University of Vienna Medical School,; Vienna Austria
Abstract:
When, in the not-so-distant past, the skin was discussed in the context of immunological reactions, it was solely viewed as a target for immunological effector systems. Recent advances have radically changed this concept of an exclusively passive role of the skin in the immune response. In fact, there now exists ample evidence that this organ functions not only as a physicochemical, but also as an immunological barrier by initiating immune responses against both exogenous pathogens and neoantigens generated in the skin itself. Dendritic, MHC class I- and class II-bearing cells in the epidermis and dermis are the principal sensitizing cells in these reactions. After antigen uptake, these cells presumably leave the skin and migrate, via the dermal lymphatics, to the regional lymph node where they present the processed antigen to the naive T cell resulting in antigen-specific T cell stimulation. T cell blasts thus generated find their way back to the skin and preferentially accumulate at the site harboring the pathogen. This selective homing mechanism is mediated by the functional interaction between skin-specific homing receptors on the surface of primed T cells and corresponding ligands on the surface of either dermal microvascular endothelial cells and/or activated keratinocytes. Upon receipt of a renewed antigenic stimulus, sensitized T cells can undergo clonal expansion resulting in the generation of effector cells/molecules sufficient in magnitude to ensure the elimination of the pathogen. According to this concept, it should be expected that a numerical and/or a functional impairment of dendritic antigen-presenting cells of the skin (eg by ultraviolet radiation or by the human immunodeficiency virus) will have deleterious consequences for the host's defense mechanisms against antigens either exogenously introduced (eg microorganisms) or newly generated (tumor antigens) in the skin. The increased frequency of cutaneous neoplasms in chronically sun-exposed individuals and in HIV-1-infected persons supports the validity of this theory.
Keywords: Dendritic Cells/IMMUNOLOGY Histocompatibility Antigens Class I/IMMUNOLOGY Histocompatibility Antigens Class II/IMMUNOLOGY Human Lymphocyte Transformation Skin/CYTOLOGY/*IMMUNOLOGY Skin Neoplasms/*IMMUNOLOGY T-Lymphocytes/IMMUNOLOGY ABSTRACT 950630
M9561169
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Important note: Information in this article was accurate in 1995. The state of the art may have changed since the publication date.
