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Sensitized human T lymphocytes are T cells that have undergone primary exposure to a specific antigen, resulting in their activation and differentiation into effector or memory cell subsets [1, 3]. These cells are fundamental to the adaptive immune system, providing a rapid and potent response upon re-exposure to the same antigen. In pathological contexts, sensitized T cells are the primary drivers of delayed-type hypersensitivity, autoimmune tissue destruction, and the rejection of transplanted organs [1, 4]. While they are frequently cited as the functional target of various therapies, they represent a heterogeneous cell population rather than a single molecular entity. Pharmacological intervention typically involves the use of small molecules or biologics that disrupt the signaling cascades required for T-cell survival and function, such as the calcineurin or mTOR pathways [2]. Consequently, monitoring the activity and frequency of these cells is crucial for managing immune-mediated diseases and ensuring the success of adoptive cell therapies. Their activation is often measured in clinical and research settings by the expression of surface markers like CD25 and the production of cytokines such as Interferon-gamma.
Immunosuppressive agents typically inhibit the activation, proliferation, or effector functions of sensitized T lymphocytes by targeting intracellular signaling pathways such as the calcineurin-NFAT pathway or the mTOR pathway, or by blocking co-stimulatory signals required for T-cell reactivation [2, 4].
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