Pattern recognition receptors (PRRs) bind molecular patterns linked to the health status of tissues. On one hand, PRRs in healthy organs inform the immune system of homeostatic cellular turn over through recognition of apoptotic cells. On the other hand, during infection PRRs induce activation of the immune system through recognition of microbial compounds in the context of tissue damage. Immune lectin receptors refer to carbohydrate-binding proteins that can fine tune immune activation by modulating signalling by canonical PRRs such as Toll-like receptors. The C-type lectin receptors (CLRs) contain a carbohydrate-recognition domain that in most cases binds sugars by ligation to Ca2+, making the sugar-binding activity Ca2+ dependent. CLRs have been implicated in recognition of a wide range of microorganisms as well as endogenous molecules. In this presentation I will provide an overview of two important C-type lectin receptors, the mannose receptor (MR, CD206) and DC-SIGN (CD209). MR and DC-SIGN lack conventional signaling motifs and tend to gear immunity away from Th1 responses. As such MR and/or DC-SIGN engagement may be exploited by pathogens as means for immunoevasion. I will describe our work towards the development of novel polymeric substances capable of inhibiting MR. These compounds have shown therapeutic potential in ischemia reperfusion injury. I will also describe our recent findings regarding the contribution of MR and DC-SIGN to recognition of bacterial biofilms which highlight the potential role of biofilm-derived carbohydrates as immune modulators.