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Patients with diabetes mellitus (DM) exhibit increased susceptibility to various infectious diseases, and DM represents a critical underlying risk factor for cryptococcosis. However, how diabetic metabolic dysregulation specifically affects host immune responses against Cryptococcus neoformans remains poorly understood. In this study, we investigated anti-cryptococcal immune responses using a streptozotocin (STZ)-induced DM model established in CnT-II transgenic mice, which harbor abundant Cryptococcus-specific CD4⁺ T cells. Inducing DM directly in these CnT-II mice enabled direct evaluation of antigen-specific immunity. DM mice, which exhibit decreased systemic reduced glutathione (GSH) under chronic hyperglycemia, showed exacerbated cryptococcal infection, characterized by significantly higher pulmonary fungal burdens, decreased IFN-γ levels, reduced survival rates, and defective granuloma formation. In vitro assays using splenocytes from uninfected DM mice revealed significantly impaired cryptococcal antigen-specific Th1 responses, expanded Treg cells, and increased PD-1 expression on CD4⁺ T cells compared with controls. Specifically, cross-combination cultures of isolated splenic CD4⁺ T cells and dendritic cells demonstrated that this Th1 impairment was intrinsic to DM-derived T cells, whereas DM-derived dendritic cells had no effect. Additionally, macrophages cultured under high-glucose conditions showed significantly decreased nitric oxide (NO) production and fungicidal activity. Importantly, exogenous GSH supplementation successfully restored both Th1 differentiation and NO production, whereas Treg cell expansion and defective macrophage fungicidal activity were GSH-independent. Taken together, our findings demonstrate how metabolic redox imbalance compromises coordinated host immunity against C. neoformans, offering potential redox-targeted therapeutic insights for diabetic hosts.