ABSTRACT
Introduction e skin permits primary immune sensitization, retains immunologic memory, and houses immunocytes, and can be preferentially a ected by T-cell malignancies. Based upon this information, Streilein proposed a speci c relationship between the immune system and the integument, much like the gut-associated lymphoid tissue [1]. He then proposed the concept of skin-associated lymphoid tissue (SALT) [2]. SALT is composed of: (1) keratinocytes, which can phagocytize, release many cytokines, and even express major histocompatability complex (MHC) class II antigens upon incubation with interferon-γ (IFN-γ); (2) epidermal Langerhans cells (LC), dendritic cells that have surface expression of MHC class II, CD1, CD3, and CD4 molecules, and are the predominant scavenger antigen-presenting cells of the epidermis; (3) skin tropic T cells, which in the epidermis include mainly “inactive” memory T cells of predominantly CD8 phenotype, although CD4 and CD4, CD8, and γδ T cells are also present; and (4) skin endothelial cells, which direct cellular tra c in and out of the skin. e epidermis contains the basic elements needed for an immune response (T cells, antigen-presenting cells, and cytokines). is, in conjunction with its anatomic structure, serves as a primary line of defense against infections. erefore, we review the components of SALT, and their interactions with viruses having cutaneous manifestations.
