Human epidermal Langerhans cells express the ICAM-3 molecule. Immunohistochemical and immunoelectron microscopical demonstration

Abstract

Three ligands have been described for the leucocyte integrin LFA-1, namely intercellular adhesion molecule (ICAM)-1, ICAM-2, and ICAM-3. ICAMs show differences in tissue distribution and inducibility. The recently described ICAM-3 is highly expressed on resting lymphocytes, monocytes and neutrophils. Here, we demonstrate that the whole human epidermal Langerhans cell (LC) population expresses this molecule. Immunohistochemical staining of skin sections with an anti-ICAM-3 monoclonal antibody displayed reactivity with dendritic epidermal cells regularly distributed along the epidermis. Highly-sensitive immunoelectron microscopy procedures, performed on freshly suspended epidermal cells both at transmission and scanning electron microscopic levels, enabled demonstration that the whole LC population expresses cell surface ICAM-3. In contrast, keratinocytes and melanocytes were consistently negative. The prominent expression of ICAM-3 by resident LC could imply a crucial part for this molecule in leucocyte-intercellular interactions in the skin.

Transcriptional profiling of human skin-resident Langerhans cells and CD1a+ dermal dendritic cells: differential activation states suggest distinct functions

“…This comparative analysis revealed that LC, residing in the epidermis under steady-state conditions, exhibit a nonstimulatory phenotype. As illustrated by Figure 2, LC display a nonmigratory profile, expressing molecules involved in cell adhesion such as Ecadherin, ICAM-3, and epidermal surface antigen or involved in DC retention such as junctional adhesion molecules and CD47 but lacking expression of molecules involved in DC migration such as CCR7 (Table 3), as also described by others [10,[33][34][35][36]. Indeed, ligation of CD47, also known as integrinassociated protein, has been demonstrated to regulate LC maturation and migration, resulting in the suppression of LC function, inhibition of T cell priming, and the subsequent inhibition of the establishment of an immune response [37].…”

The Effects of Inflammatory Cytokines on the Isolated Human Sebaceous Infundibulum

“…MHC class I was constitutively expressed, particularly on the basal cells of infundibula, and was apparently unaffected by exogenous cytokines (Table I). ICAM-3 was not constitutively expressed by keratinocytes or in response to exogenous cytokines (Table I); however, individual cells were seen to stain with ICAM-3 that we attribute to the presence of Langerhans cells (Manara et al, 1996). PMA for 24 h stimulated both ICAM-1 and HLA-DR expression in all infundibula (Table I); however, by 3 d, PMA treated infundibula expressed neither ICAM-1 nor HLA-DR (Table I).…”

Imiquimod, a Topical Immune Response Modifier, Induces Migration of Langerhans Cells11The authors have declared a conflict of interest.

“…These changes are thought to facilitate migration of Langerhans cells from skin to DLN and are indicative of activated Langerhans cells (Larsen et al, 1990;Kondo and Sauder, 1995) and are thought to involve downregulation of E-cadherin (Borkowski et al, 1994;Jakob and Udey, 1998). Following activation, Langerhans cells express a number of cell surface markers including B7, ICAM-1, and ICAM-3 and increase their expression of major histocompatibility complex (MHC) class II antigens (Shimada et al, 1987;Aiba and Katz, 1990;Tang and Udey, 1991;Manara et al, 1996;Laihira and Jansen, 1997). As Langerhans cells play a crucial part in immunosurveillance there has been considerable interest in agents that modify Langerhans cell function (Simon et al, 1992;Bacci et al, 1996;Ozawa et al, 1996;Qu et al, 1997).…”