C-type lectin receptors (CLRs) present on myeloid cells provide crucial signals for the induction of innate and adaptive immune responses. Their broad ligand specificity places them in a perfect position to sense both microbial intruders and signs of tissue injury or cell death. In this article, we review the mechanisms that link CLR engagement to tailored cellular responses against those perceived threats. We discuss not only how molecular interplay between signaling by CLRs and by other pattern recognition receptors fine-tunes host-protective responses but also how these receptors can lead to pathological immune responses. An understanding of how these responses are regulated may offer strategies for treating not just infectious diseases but also autoimmune or malignant disorders.
Gringhuis et al. (Tue,) studied this question.