Epidermal Langerhans cells in infectious diseases

Abstract

Paul Langerhans was one of the most brilliant scientific observers of his time, contributing considerably not only to medicine but also to zoology by describing new species of invertebrates (De Panfilis, 1988). He was a medical student at the Berlin Pathological Institute when he discovered in 1868 the epidermal cells that bear his name. He believed that these gold chloride-positive midepidermis dendritic cells were intra-epidermal receptors for extracutaneous signals to the nervous system (Langerhans, 1868). This neural hypothesis prevailed for almost a century. Not until 1965, when the morphological identity between Langerhans cells (LC) and histiocytes X cells was described, was a possible mesenchymal derivation for LC postulated (Basset and Turiaf, 1965). In 1966, Campo-Aasen and Pearse demonstrated cytochemically that epidermal LC share specific enzymes with macrophages. Further accumulated evidence supported the striking similarities between LC and macrophage/monocytes, including the expression of Fc and C3 receptors (Stingl et al., 1977), expression of Major Histocompatibility Complex class I1 (Ia) molecules (Klareskog et al., 1977; Rowden et al., 1977), ability to migrate (Silberberg, 1973) and the in vitro ability to stimulate allogeneic T-cells (Stingl et al., 1978). LC also produce interleukin-1 (IL-l), previously denoted in the skin as epidermal cell-derived thymocyte-activating factor (ETAF) (Sauder et al., 1984). The IL-1 serves as the second signal in triggering the production of interleukin-2 (IL-2) by T-helper cells, thus amplifying ongoing T-cell responses.