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Autologous expanded Tregs are a cell therapy product consisting of regulatory T cells (Tregs) that are isolated from a patient's own blood and then expanded ex vivo (outside the body) to achieve sufficient numbers for therapeutic infusion. These CD4+CD25+FOXP3+ regulatory lymphocytes play a critical role in maintaining immune tolerance and suppressing aberrant immune responses. The expansion process typically involves stimulation with anti-CD3/anti-CD28-coated beads and interleukin-2 (IL-2), resulting in highly pure (>90% FOXP3+) populations with potent immunosuppressive function[1][5][6]. Upon reinfusion into the patient, these cells can modulate immune activity through multiple mechanisms including direct suppression of effector T cell proliferation, modulation of antigen-presenting cells, secretion of immunosuppressive cytokines (such as IL-10), and induction of endogenous antigen-specific tolerance[1][2][5]. Autologous expanded Treg therapies have been investigated in clinical trials for autoimmune diseases such as type 1 diabetes, amyotrophic lateral sclerosis (ALS), idiopathic aplastic anemia, organ transplantation tolerance induction, and other inflammatory or immune-mediated conditions[4][5][6][8]. The approach is designed to minimize risk of rejection by using the patient’s own cells while aiming to restore homeostasis without broad systemic immunosuppression.
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