Invasive fungal infections, including candidiasis, account for ~1.5 million deaths per year worldwide. Candidiasis is the fourth most common healthcare-associated infection, killing more people per year than TB or malaria. Several strains of Candida cause candidiasis however >95% of Candida infections are caused by C. albicans (54%), C. glabrata (19%), C. tropicalis (11%) and C. parapsilosis (11%). Current anti-fungal therapies are often insufficient, as the mechanisms regulating anti-fungal immunity are not fully understood. Fungal infections cause a complex immune response involving complement receptors (CRs), C-type lectin-like receptor (CLRs), Toll-like receptors (TLRs) and others. A better understanding of anti-fungal immunity is required to develop novel immunotherapies. To examine the importance of CLRs in antifungal immunity, we have performed a comprehensive analysis of the role of Dectin-1 and Mincle in different myeloid cells in response to Candida. Expression levels of Dectin-1 and Mincle on bone marrow derived macrophages (BMDM), bone marrow derived dendritic cells (BDMC) and neutrophils were measured by flow cytometry and compared. BMDM and BMDC from WT, Dectin-1 deficient and Mincle deficient mice were cultured and cytokine production (TNF, IL-1b, IL-10, IL-12p40 and IL-6) in response to Candida was measured. Dectin-1 deficient cells show reduced cytokine production. WT, Dectin-1 deficient and Mincle deficient mice were infected with a low and high dose of C. albicans and T cell responses (IFN-g and IL-17), fungal burden and survival were measured. Again, Dectin-1 is important for cytokine production from the different myeloid cell populations, T cell responses and survival. The role for Mincle during C. albicans infections is more subtle, however we have observed small effects from Mincle in the different aspects of anti-fungal immunity.