Functional Expression and Modulation of C5a Receptor (CD88) on Skin Dendritic Cells

Abstract

The process of differentiation of resident epidermal Langerhans cells (LC) generates: i) changes in the level of expression and repertoire of cell surface molecules; ii) a decrease in the antigen processing capacity; iii) a significant increase in the ability to present peptides to T cells; and iv) the mobilisation of dendritic cells (DC) from the epidermis towards the draining lymph nodes¹. There is little information about the factors involved in DC migration from non-lymphoid peripheral tissues as part of the process of skin DC differentiation. “In vivo” studies demonstrated that the administration of lipopolysaccharide (LPS), Tumour Necrosis Factor (TNF) α or Interleukin 1 (IL-1) can trigger the trafficking of DC from non-lymphoid tissues (i.e. skin, lung, gut, heart and kidney) towards secondary lymphoid organs^2–7. A similar situation is observed in the inflammatory reaction that takes place during the first three days after skin transplantation; or after short term culture of skin organ explants⁸. In both cases it is likely that the skin injury by itself releases inflammatory mediators, sufficient to trigger both phenotypic and functional DC changes and migration of completely or partially mature skin DC.