Thyrotropin receptor-specific autoreactive T cells (TSHR-specific T cells)

Autoreactive T cells recognizing Graves’ disease–associated self-antigen epitopes, primarily those derived from the thyrotropin receptor (TSHR), are the central orchestrators of the autoimmune response in Graves' disease [1]. These T cells, particularly those with Th1 and Th17 profiles, recognize specific TSHR peptide fragments presented by MHC class II molecules on antigen-presenting cells [2]. Their activation leads to the production of pro-inflammatory cytokines and provides the necessary signals for B cells to produce thyroid-stimulating immunoglobulins (TSI), which cause hyperthyroidism and the extrathyroidal manifestations of the disease, such as Graves' ophthalmopathy [3]. Therapeutic strategies targeting these cells, such as the investigational drug ATX-GD-59, utilize soluble, non-processed peptides (apitopes) to induce immunological tolerance [4]. By binding directly to MHC molecules in the absence of costimulatory signals, these agents aim to induce anergy or apoptosis in the pathogenic T-cell population, thereby halting the autoimmune process without the risks associated with broad immunosuppression [5].

Other names

Autoreactive T cells recognizing Graves’ disease–associated self-antigen epitopesGraves' disease-associated T cellsThyroid-reactive T lymphocytesTSHR-reactive T cells

Antigen-specific immunotherapy via induction of immunological tolerance (anergy or deletion) in TSHR-specific T cells.