The innate ability of macrophages to induce an immune response to pathogens is dependent upon germline encoded pattern recognition receptors which recognise conserved microbial structures. These receptors not only mediate pathogen recognition, but promote microbial uptake and killing and the induction of inflammatory responses. Although the recently described Toll-like receptors (TLR) have been shown to play a central role in mediating the intracellular signals involved, the non-TLRs also have important functions in these processes. Once such receptor is Dectin-1, a myeloid expressed signalling C-type lectin-like receptor which is involved in the innate recognition of fungal pathogens. Dectin-1 can induce a variety of cellular responses, including phagocytosis, the respiratory burst and cytokine production. These responses are mediated through novel signalling pathways induced from the cytoplasmic immuno-receptor tyrosine based activation-like motif of the receptor. Although the in vivo role of Dectin-1 has still to be fully elucidated, there is emerging evidence that this receptor plays a role in the inflammatory response to pulmonary fungal pathogens and that it is involved in certain autoimmune and respiratory diseases.