Together with the report that homozygosity for the common P1104A TYK2 allele selectively impairs cellular responses to IL-23 and underlies TB and MSMD with high and low penetrance, respectively (9, 12, 48), these findings suggested that human IL-23 is required for optimal IFN-γ-dependent immunity to mycobacteria, but redundant for optimal IL-17-dependent immunity to C. albicans (11). This evidence concerns the gene IL23A and Mendelian susceptibility to mycobacterial diseases.