Abstract
Pentraxins are soluble innate immunity receptors involved in sensing danger molecules. They are classified as short (CRP, SAP) and long pentraxin subfamilies, including the prototypic long pentraxin PTX3. Pentraxins act mainly as bridging molecules favoring the clearance of microbes and dead cells. They are also involved in many other biological processes, such as regulation of complement activation, inflammation and tissue homeostasis. Autoantibodies directed against pentraxins have been reported in various autoimmune diseases, especially in systemic lupus erythematosus and ANCA-associated vasculitis. In this review, we review the main biological characteristics and functions of pentraxins and summarize data concerning autoantibodies directed against pentraxins in the context of autoimmune diseases and discuss their potential pathological role.
Highlights
The innate immune system is involved in many physiological processes, including antimicrobial defence, inflammation, initiation and regulation of adaptive immunity and maintenance of tissue homeostasis [1]
Pentraxins are soluble PRM involved in antimicrobial defense and efferocytosis
A tolerance breakdown to pentraxins has been evidenced during various autoimmune diseases
Summary
The innate immune system is involved in many physiological processes, including antimicrobial defence, inflammation, initiation and regulation of adaptive immunity and maintenance of tissue homeostasis [1]. The detection of danger signals by innate immunity receptors is crucial in initiating appropriate immune responses that are fine-tuned to the motifs encountered (tolerance to self, protection against non-self) These receptors are highly conserved molecules called Pattern Recognition Receptors (PRR). Soluble PRM act as bridging molecules, linking extracellular DAMPs and PAMPs with cell associated PRR They include collectins, ficolins, some complement family proteins, soluble forms of membrane PRR (such as soluble scavenger receptors and C-type lectins released after shedding of the membrane forms), and by pentraxins. As their membrane counterparts, sPRM are highly conserved and bind a variety of ligands expressed by microbes and altered/modified self. We raise hypothesis on the potential pathological role(s) of antipentraxin autoantibodies
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