| There has been a recent surge of interest in innate immunity and identifying the mechanisms by which this evolutionary ancient arm of the immune system distinguishes self from non-self. This research has led to the understanding that innate recognition of non-self is in large part, mediated through germ-line encoded molecules, known as "pattern recognition receptors", that recognize conserved microbial structures (1). In particular, the discovery of the Toll-like receptors, a class of receptors endowed with this role (1), has allowed significant insights into how anti-microbial inflammatory signals are generated. Despite these advances in understanding responses to bacteria, much less is known about the innate responses to fungal pathogens or their components, even though fungal infections are frequent worldwide in immunocompromised individuals and account for over 10% of all hospital-acquired (nosocomial) infections (2). The studies presented in this work address the innate recognition of one conserved fungal component, beta (beta)-glucan, and begin to elucidate signaling mechanisms used by human polymorphonuclear leukocytes to respond to this polysaccharide. |
