CLEC7A and infection: Given the proband’s history of infections and/or antibody responses to microbes known to bear DECTIN-1 ligands (Saccharomyces, Candida, Salmonella, and Clostridium) and unusually severe enteritis, the CLEC7A L183F allele emerged as a promising candidate to increase expressivity of the CTLA4 allele and/or modify the IDAIL phenotype.