The complement system is an innate immune defense machinery comprising components that deploy rapid immune responses and provide efficient protection against foreign invaders and unwanted host elements. The complement system is activated upon recognition of pathogenic microorganisms or altered self-cells by exclusive pattern recognition molecules (PRMs), such as collectins, ficolins and pentraxins. Recent accumulating evidence shows that the different classes of effector PRMs build up a co-operative network and exert synergistic effects on complement activation. In this review, we describe our updated view of the crosstalk between previously unlinked PRMs in complement activation and the potential pathogenic effects during infection and inflammation. Crosstalk between various immune defense factors helps the body mount a rapid response against foreign invaders but can also lead to disease. In a review article, Ying Jie Ma from the University of Copenhagen, Denmark, and colleagues provide an overview of the key pattern-recognition molecules that work together to activate the complement system, a set of over 20 different proteins in the blood that, when spurred into action, helps destroy pathogens and eliminate infections. These pattern recognizers collaborate to produce synergistic effects in immune recognition, response and resolution. However, as well as being protective, they can also cause disease; for example, they can trigger arthritis following infection with chikungunya virus or Ross River virus. These proteins may therefore be suitable targets for drug therapies designed to ameliorate complications associated with certain infections.
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Jie et al. (2017) studied this question.
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