Background Tuberculosis (TB) is an infectious disease that poses a significant health threat and is one of the leading causes of death worldwide. Diabetes mellitus (DM) has high morbidity and mortality rates. Previous studies have reported that comorbidities can influence one another and aggravate immune disorders. A systematic and comprehensive evaluation of the immune status of patients with TB and DM (TB-DM) is helpful for early clinical immune intervention and for promoting the recovery of patients with TB-DM. Methods This study included 159 patients with TB without DM (TB-NDM) and 168 patients with TB-DM. Interferon-γ (IFN-γ) release assays (IGRAs) and TB-specific antibodies against 38kD+16kD proteins were used to detect humoral and cellular immune responses. Flow cytometry was used to analyze the absolute counts of the lymphocyte subsets. Results There was no significant difference in the positive rate of enzyme-linked immunospot (ELISPOT) assays, enzyme linked immunosorbent assay (ELISA), and 38kD+16kD antibodies between the TB-DM and TB-NDM groups. Pulmonary lobe lesion and cavity formation rates were significantly higher in patients with TB-DM with poor glycemic control than patients with TB-NDM and TB-DM with normal glycemic control. The absolute counts of T lymphocytes, CD8+ T lymphocytes, and B lymphocytes in patients with TB-DM were markedly lower than those in patients with TB-NDM. The absolute counts of T lymphocytes and CD8+ T lymphocytes in patients with TB-DM and hyperglycemia were lower than those in patients with euglycemia. Linear regression analysis revealed that the absolute counts of total T lymphocytes, CD8+ T lymphocytes, and NK cells in patients with TB-DM significantly decreased with increasing fasting blood glucose (FBG) levels. Conclusion Hyperglycemia is a risk factor for pulmonary cavity formation and lobe lesions in patients with TB-DM and suppresses the absolute counts of total T lymphocytes, CD8+ T lymphocytes, and NK cells in patients with TB-DM. The potential mechanism may involve the downregulation of innate and adaptive immune responses.