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The Dendritic cell–T cell axis is the fundamental interface of the adaptive immune system, facilitating the transition from innate to specific immunity (Banchereau & Steinman, 1998, Nature). Dendritic cells (DCs) function as professional antigen-presenting cells that capture, process, and present antigens to T cells via Major Histocompatibility Complex (MHC) molecules (Mellman & Steinman, 2001, Cell). This interaction requires a complex synapse involving primary TCR-MHC signaling and secondary co-stimulatory or co-inhibitory signals, such as the CD80/86-CD28 and PD-L1-PD-1 pathways (Sharpe & Freeman, 2002, Nature Reviews Immunology). In oncology, the axis is often suppressed by the tumor microenvironment, leading to T cell exhaustion and immune evasion (Pardoll, 2012, Nature Reviews Cancer). Conversely, in autoimmune diseases, inappropriate activation of this axis leads to the destruction of healthy tissues. Pharmacological modulation of this axis is a cornerstone of modern medicine, exemplified by immune checkpoint inhibitors that reinvigorate T cells by blocking inhibitory signals. Other therapies, such as CTLA-4-Ig fusion proteins like abatacept, target the axis to induce immunosuppression in transplant or rheumatological settings. Dendritic cell-based vaccines also leverage this axis by priming the immune system to recognize specific pathogens or malignant cells.
Modulation of the immunological synapse through the inhibition or activation of co-stimulatory and co-inhibitory signaling molecules during antigen presentation.
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