Innate-like T cells such as γδ T cells, natural killer T (NKT) cells and mucosal-associated invariant T (MAIT) cells are a major component of the immune system, however the cytokine signalling pathways that control their development and function in humans are unknown. Primary immunodeficiencies caused by single gene mutations provide a unique opportunity to investigate the role of specific molecules in regulating human lymphocyte development and function. Autosomal dominant-hyper IgE syndrome (AD-HIES) is caused by heterozygous loss-of function mutations in STAT3. STAT3 signals downstream of many cytokine receptors, including those for IL-6, IL-10, IL-21, and IL-23. We used lymphocytes from these patients to assess the roles of STAT3 in innate-like T cell differentiation in vivo and in vitro. Patients with STAT3 mutations had reduced numbers of peripheral blood MAIT and NKT cells. Analysis of STAT3 mosaic individuals revealed that this effect was cell intrinsic. Surprisingly, the residual STAT3-deficient MAIT cells expressed normal levels of the transcription factor RORγt. Despite this they had defective secretion of IL-17A and IL-17F, but were able to secrete normal levels of cytokines such as IFNγ and TNFα. To determine which cytokine receptors were required upstream of STAT3 we examined patients with loss-of function mutations in IL12RB1 and IL21R and found decreases in for MAIT and NKT cells, respectively. Thus, this reveals for the first time the essential role of STAT3 signalling downstream of IL-23R and IL-21R in controlling human MAIT and NKT cell numbers.