Diabetes type 1 is a chronic autoimmune disease in which insulin-producing cells located in the pancreatic islets of Langerhans are gradually destroyed by autoreactive T cells. Quantitative or qualitative dysfunctions in naturally arising CD4+Foxp3+ T lymphocytes may result in ineffective suppression of autoreactive T cells. CD62L is a surface molecule that plays role in homing capabilities of Tregs in autoimmunity if they must be present in the target tissue in order to have the proper effect. Only cells with high expression of CD62L are able to protect against diabetes. We investigated CD4+Foxp3+ cells expressing CD62L after in vitro stimulation with anti-CD3 from children with long-standing diabetes type 1 and we found lower frequencies of these cells in diabetic group compared to their healthy counterparts.