Dyslipidemia, characterized by altered lipid profiles, is a major risk factor for cardiovascular disease and has also been linked to dysregulated immune responses in autoimmune inflammatory diseases and during infections. Given that group 1 CD1-restricted T cells recognize lipid antigens, we hypothesized that hyperlipidemia may alter their activation and function. To test this, we utilized two TCR transgenic mouse models, HJ1Tg (CD1b autoreactive) and DN1Tg (CD1b/mycolic acid-specific), on a human group 1 CD1 transgenic (hCD1Tg) and LDLR-deficient background to examine the effects of diet-induced dyslipidemia on group 1 CD1-restricted T cells under homeostatic and infectious conditions. HJ1Tg/hCD1Tg/LDLR-/- mice fed a high-fat diet (HFD) developed progressive weight loss and severe skin inflammation. HJ1 T cells from HFD-fed mice exhibited an activated phenotype and produced elevated IL-17A at baseline compared to normal chow (NC)-fed controls. Notably, skin inflammation was significantly reduced after switching to NC, suggesting that hyperlipidemia drives chronic activation of autoreactive CD1b-restricted T cells, contributing to inflammatory disease. In contrast, HFD-fed DN1Tg/hCD1Tg/LDLR-/- mice did not develop spontaneous dermatitis. Instead, DN1 T cells exhibited enhanced IFN-γ production and mycobacterial clearance in vitro, linked to increased TCR signaling and glycolysis, independent of changes in dendritic cell antigen presentation. However, dyslipidemia also increased apoptosis of DN1 T cells, potentially compromising their ability to control M. tuberculosis infection in vivo. These findings demonstrate that hyperlipidemia affects both autoreactive and microbial lipid-specific group 1 CD1-restricted T cells, with distinct outcomes influenced by TCR specificity.