Type 2 diabetes (T2D) remission, defined as achieving a hemoglobin A1c (HbA1c) <6.5% without antihyperglycemic agents for >3 months, through dietary weight loss approaches is an emerging practice in diabetes care. However, little is known about how the immune system responds to remission interventions with structured medication reduction. Thus, we explored changes in immune cell phenotype and function after a 12-week nutritional intervention in a sub-sample of participants from the DiEt ChoIce to promote type 2 Diabetes rEmission (DECIDE) study. Seventeen participants (9 female/8 male; age 62.5 ± 10.7 years) were recruited, with 13 self-selecting a low-carbohydrate diet (<50 g carbohydrate/day) and four selecting a low-calorie diet (~900 kcal/day). The intervention led to significant weight loss of 6.4 kg (p<0.001) and a reduction in HbA1c of 0.9% (p<0.001). Antihyperglycemic agents were reduced, with 85% of medications deprescribed by week 12. Despite these clinical improvements, no changes were observed in the proportion of classical (89.1 ± 3.4% vs. 88.9 ± 4.6%; p=0.77), non-classical (7.5 ± 2.0% vs. 7.6 ± 3.1%; p=0.85), and intermediate (3.3 ± 1.5% vs. 3.4 ± 1.6%; p=0.65) monocyte populations. Monocyte toll-like receptor 4 (TLR-4) expression and neutrophil oxidative burst in response to lipopolysaccharide were unchanged. Similar levels of inflammatory markers, including monocytes (4.3 × 10³ vs. 4.3 × 10³ cells/µL; p=0.887), neutrophils (4.7 × 10³ vs. 4.2 × 10³ cells/µL; p=0.104), and plasma C-reactive protein (1.8 vs. 2.1 mg/L; p=0.287), corroborated these findings. Despite significant weight loss and improved glycemic regulation, 12 weeks of a low-carbohydrate or low-calorie diet with medication reduction resulted in no significant changes in monocyte phenotype, neutrophil oxidative burst, immune cell counts, or circulating inflammatory markers. These exploratory data suggest that inflammation may not track weight loss in T2D and highlight the need to better understand the influence of concomitant medication reduction on immune markers during remission interventions.