The presence of autoantibodies against oxidized low-density lipoprotein (oxLDL) in the lesions of patients with atherosclerosis provided the initial evidence of the involvement of adaptive immunity in the development of atherosclerosis. Patients with type 2 diabetes mellitus (T2DM) often have autoantibodies to oxLDL, and thus platelet-derived microparticles (PDMPs), macrophages, lymphocytes, and anti-oxLDL antibodies could all play important roles in the development of atherosclerosis in patients with T2DM. Soluble cytotoxic T-lymphocyte-associated antigen 4 (sCTLA-4) can modulate and terminate immune responses and is elevated in patients with some autoimmune disorders. However, sCTLA-4 levels have not previously been investigated in patients with T2DM. We investigated the levels of transforming growth factor (TGF)β₁ and sCTLA-4 in T2DM patients to determine the clinical association between TGFβ₁ and sCTLA-4. The levels of C-reactive protein (CRP), monocyte chemoattractant protein-1 (MCP-1), soluble P-selectin (sP-selectin), soluble E-selectin (sE-selectin), soluble vascular cell adhesion molecule-1 (sVCAM-1), PDMP, TGFβ₁ and sCTLA-4 were higher in T2DM patients than in non-diabetic controls. The patients with high TGFβ₁ exhibited a significant increase in PDMP, MCP-1, sP-selectin, sE-selectin, sVCAM-1 and sCTLA-4 compared with those with low TGFβ₁. In contrast, anti-oxidized low-density lipoprotein immunoglobulin G (anti-oxLDL IgG) was significantly decreased in T2DM patients with high TGFβ₁. In addition, PDMP levels were positively correlated with sCTLA-4 and negatively correlated with anti-oxLDL IgG. These results suggest that PDMP, TGFβ₁ and sCTLA-4 can partially modulate immune responses in T2DM patients, resulting in the decrease in anti-oxLDL IgG and development of atherosclerosis.