Apoptosis pathway in T cells

The apoptosis pathway in T cells is a fundamental biological process responsible for maintaining immune system balance and preventing autoimmunity (StatPearls, "Apoptosis"). It primarily operates through two distinct but converging routes: the extrinsic pathway, initiated by death receptors such as Fas (CD95), and the intrinsic pathway, which is regulated by the Bcl-2 family of proteins at the mitochondria (PubMed, PMID: 29958164). In T cells, these mechanisms are crucial for negative selection in the thymus and activation-induced cell death (AICD) in the periphery to eliminate redundant or self-reactive cells (NIH, "Immune System"). Dysregulation of T-cell apoptosis is a hallmark of various diseases; for instance, insufficient apoptosis can lead to autoimmune lymphoproliferative syndrome (ALPS), while excessive apoptosis is seen in HIV/AIDS (PubMed, PMID: 11244030). Pharmacological intervention often targets specific nodes within this pathway, such as using Bcl-2 inhibitors like Venetoclax to treat T-cell malignancies or corticosteroids to induce T-cell death in inflammatory conditions (PubChem, "Venetoclax"). Therapeutic strategies also include modulating death receptor signaling to enhance anti-tumor immunity or prevent graft-versus-host disease (PubMed, PMID: 25611152). Understanding the balance between pro- and anti-apoptotic signals is vital for developing precision medicines that can selectively eliminate pathogenic T cells while sparing healthy ones.

Other names

Programmed cell death in T lymphocytesT-cell apoptosis signalingActivation-induced cell death (AICD)T-lymphocyte apoptotic process

Drugs targeting this pathway typically act by inhibiting anti-apoptotic proteins (e.g., Bcl-2 inhibitors), activating death receptors (e.g., Fas agonists), or modulating upstream signaling to induce or prevent T-cell death.