Figure 1.

Cells, cytokines, and the complement system are involved in skin homeostasis. Keratinocytes recognize pathogen-associated molecular patterns via pattern recognition receptors on their surfaces, and they secrete antimicrobial peptides. Fibroblasts secrete C3b, C5a, and MAC, which are involved in pathogen clearance by complement. Langerhans cells are antigen-presenting cells for microbial antigens in the epidermis. Dendritic cells secret most components of complement system and mediate together with macrophages pahgocytosis of pathogens via complement receptors (CR1, CR3 and CR4). They could mediate phagocytosis in the clearance of pathogens by receptors (e.g., C3R, C4R) on their surface in turn. Macrophages participate in inflammation and wound repair. Receptors for C3a on mast cells can be activated by their ligands to degranulate and secret cytokines including MCP-1 and RANTES, which participate in wound repair. Pathogens stimulate collectins to activate complement system. Collectins may also modulate inflammation by macrophages and DCs directly. Keratinocytes recruit αβ T cells, and γδ T cells to epidermis. AMP, antimicrobial peptide; PRR, pattern recognition receptor; APC, antigen-presenting cell; DC, dendritic cells.