Redundancy and robustness versus division of labour and specialization in innate immunity

Apparent redundancy is a recurrent theme in innate immunity in various domains including inflammatory cytokines, chemokines and pattern recognition receptors. While sharing core function, different mediators may subserve distinct functions related for instance to production and release (e.g. IL-1 alpha versus IL-1 beta), predominantly local versus systemic function (e.g. PTX3 versus C-reactive protein) or fine tuning of innate and adaptive responses (chemokines). Based on hard-wired phagocyte recruitment and regulation by a wide spectrum of chemokines and conventional or atypical receptors, I argue that trafficking of phagocytic cells is a robust output of the chemokine system, resistant to genetic or environmental variation. In general, I speculate that the apparent overlap and redundancy observed in core functions represents an evolutionary strategy to preserve robust essential core outputs in the face of genetically or environmentally caused variation.