Pattern recognition molecules and innate immune evasion

Pattern recognition molecules (PRMs) are crucial in host mediated innate immunity and the initiation of adaptive immunity against invading pathogens. Depending on the invading pathogen, PRMs become activated by the recognition of pathogen-associated molecular patterns (PAMPS) and mediate pathogen killing. C-type lectin receptors function as pattern recognition receptors (PRRs) and the transmembrane receptor dectin-1 recognizes specific β-1,3-linked glucans expressed by several fungal pathogens. The cytosolic nucleotide binding oligomerization (Nod)-like receptors (NLRs), including Nod1 and Nod2, sense specific intracellular microbials of bacterial origin. Pathogen recognition mediated by dectin-1 or Nod1 and Nod2 results in the activation of nuclear factor-κB (NF-κB) mediated gene expression and thereby the induction of protective immune responses. To circumvent the killing attacks of the host, pathogens have evolved different evasion strategies for successful survival, including the induction of impaired recognition and the induction of impaired immune responses. In addition to extracellular and intracellular PRRs, peptidoglycan recognition proteins (PGRPs) are highly conserved PRMs. The human PGRP family consists of four members, subdivided into three bactericidal proteins and one amidase that hydrolyzes bacterial peptidoglycan to reduce pro-inflammatory responses. An increased resistance of pathogens to PGRPs might be related to evasion strategies to escape host immune responses