Antigen-presenting cells (APC), such as dendritic cells (DCs) and macrophages, are located throughout the body to sense and capture invading pathogens and to trigger immune responses to fight such invaders. In addition, in the absence of danger signals, DCs have an active role in the induction of T cell tolerance and the maintenance of homeostasis. The recognition and internalization of pathogens is mediated by so-called pathogen-recognition receptors, germ-line encoded cell surface receptors that include toll-like receptors (TLR) and C-type lectins (CLR). It is becoming increasingly clear that during the long co-evolution with their hosts, pathogens have evolved mechanisms to misuse pathogen-recognition receptors to suppress or evade immune responses and thus to escape clearance. In this chapter, we will review recent examples of how pathogens evade immune activation by targeting recognition receptors on APC and subverting their function.
BACTERIAL RECEPTORS ON ANTIGEN-PRESENTING CELLS
APC interact with invading pathogens via pathogen-recognition receptors that bind conserved patterns of carbohydrates, lipids, proteins and nucleic acids in classes of microbes. This variety of receptors and conserved ligands recognized ensures that most, if not all, microbes can be detected by the immune system, either by a single or by combinations of receptors. Pathogen-recognition receptors include TLR and CLR (Figure 9.1). To date, 11 TLR have been identified (see Chapter 2) that each targets specific pathogenic structures, such as lipopolysaccharide (TLR4), viral dsRNA (TLR3) and bacterial peptidoglycans (TLR2/TLR6).