In addition to bacterial and synthetic lipids, mammalian self-lipids can function as antigens for type I NKT cells in homeostasis and in sterile inflammation. We recently reported that CD1d preferentially binds to sphingolipids (Huang et al. Cell, 2023), and that self-sphingolipids lacking carbohydrate or phosphate headgroups can also act as CD1d ligands for the murine 2C12 type 1 NKT cell receptor (Abstract Cheng et al.). Here we ask whether human type I NKT cell T cell receptors can bind and recognize the headless lipid ceramide presented by CD1d. CD1d tetramers treated with long chain C42:2 ceramide strongly stain about half of the type I NKT cells in human peripheral blood, as well as several primary type I NKT cell clones and polyclonal cell lines. These data de-emphasize the role of carbohydrate or phosphate head group recognition and support models in which molecules with small or absent head groups allow TCR and CD1d contact. Ceramide and sphingomyelin, which are the two core members of the sphingomyelin cycle that reads out cellular stress, are now both implicated in type I NKT homeostasis. Although CD1d-ceramide-TCR interactions were reproducibly detectable, low or undetectable activation in vitro was seen in ceramide-challenges with antigen presenting cells, raising further questions about co-stimulation requirements, or even a possible role of headless self-lipids in positive selection or maintenance of NKT cells in tissues.