The involvement of CS/DS in inflammation has been extensively explored, whereas the role of IdoA is not well defined 43,44. The inflammatory response initiated by infection or injury results in diverse processes, involving cell recruitment, extravasation and cell/pathogen clearance. For example, during wound healing, CS/DS is reported to be the dominating GAG in wound fluid 45,46. FGF2 and FGF7 are two important growth factors during wound repair and they have been shown to preferentially bind to IdoA-containing motifs in CS/DS, promoting proliferative processes (Fig. 4A,F). CS/DS has been proposed, in combination with FGF-10, as a pharmacological accelerator of wound closure as a result of its capacity to stimulate re-epithelialization 47. CS/DS can potentially affect several steps during cell recruitment. For example, CS/DS has been shown to interact with P-selectin, which is expressed on endothelial cells and platelets 48 (Fig. 4E). CS/DS is reported to influence the recruitment of polymorphonuclear cells in a thioglycollate-induced inflammatory model in a supposedly P-selectin manner 49. RANTES, a leukocyte-recruiting chemokine, also interacts with IdoA-containing segments in CS/DS 50. An essential step during extravasation is the
