Prologue: The Various Facets of Innate Immune Effector Responses
The Prologue of Part VI addressed the various facets of innate immune effector responses which characterize the first line of our defense system. Inflammatory responses committed to combating both infective and sterile tissue injury rank first which consists of numerous cellular, humoral, and molecular pathways. Quite often, stress responses merge into and interact with those inflammatory responses. The process of innate immune inflammation emerged over millions of years during evolution, is complex and multifaceted, and passes through several stages. In a way, all possible tools of the innate immune system are getting involved when activated by MAMPs and/or DAMPs; for example, intracellular PRM-triggered signalling pathways play a crucial role in DAMP-promoted inflammation-mediated host defense. An integral part of the inflammatory scenario is the process of phagocytosis that can be regarded as a key mechanism of innate immunity. It is responsible for removal of pathogens and host damaged/dying cells and, thus, plays a dominant role in the resolution phase of inflammation. However, cellular effector responses are not alone on the vast battlefield; they are accompanied by MAMP/DAMP-induced humoral innate effector responses which provide effective support. They include the complement system that is supported by several co-players such as collectins and ficolins and receives valuable help from the group of antimicrobial peptides. Certainly, all the robust DAMP-promoted PRM-triggered cellular and humoral inflammatory defense responses bear the risk of self-destructive uncontrolled overreaction. For this reason, evolution has created multi-level regulatory mechanisms including epigenetic modifications to ensure tight, context-specific, and appropriately pitched pathways restricted to their intrinsic nature of defense of the individual.