Immune system modulation via antigen-specific tolerance induction

"Immune system modulation via antigen-specific tolerance induction" does not refer to a single molecule, receptor, enzyme, or protein. Instead, it describes a therapeutic strategy aimed at selectively suppressing pathological immune responses against specific antigens while preserving overall immunity. This approach is central to the treatment/prevention of autoimmune diseases and allergies. Mechanistically, this process involves several cellular players—most notably **regulatory T cells** (FOXP3+ iTregs/nTregs; Tr1; Th3) that are induced either centrally in the thymus or peripherally upon exposure to specific antigens presented under non-inflammatory conditions. **Dendritic cells** play a pivotal role when they present antigens with low co-stimulatory signals or express inhibitory molecules like PD-L1/PD-L2. Regulatory B cells also contribute through secretion of IL‑10/TGF‑β. Therapeutic approaches include administration of tolerogenic nanoparticles loaded with disease-relevant peptides/proteins, engineered DNA plasmids encoding self-antigens, peptide-based therapies, and ex vivo–generated tolerogenic dendritic cell infusions. These interventions aim to expand antigen-specific regulatory populations while deleting/anergizing pathogenic effectors. This entry should be considered "incorrect" as a canonical target because it refers broadly to an *immunological process* rather accurate for structured drug-target databases.

Other names

Antigen-specific immune toleranceAntigen-specific tolerance inductionImmune tolerance inductionTolerogenic immune modulation

Induction and expansion of regulatory T cells (Tregs), including FOXP3+ iTregs and IL‑10–producing Tr1 cells. Promotion of effector T cell anergy or deletion by tolerogenic dendritic cells through low co-stimulation or inhibitory signals such as PD-L1/PD-L2 and CTLA‑4 interactions. Secretion of immunosuppressive cytokines such as IL‑10 and TGF‑β by regulatory B cells and other regulatory subsets to suppress effector responses.