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Dendritic cells and T cells represent a fundamental cellular interaction in the immune system rather than a single molecular target. Dendritic cells (DCs) function as professional antigen-presenting cells (APCs) that bridge innate and adaptive immunity by capturing antigens and presenting them to T cells via Major Histocompatibility Complex (MHC) molecules (Banchereau & Steinman, 1998, Nature). This interaction, known as the immunological synapse, is regulated by various costimulatory and coinhibitory molecules that determine the magnitude and quality of the T cell response (Worbs et al., 2017, Nature Reviews Immunology). In cancer, the DC-T cell axis is often suppressed, leading to immune evasion, while in autoimmune diseases, it is inappropriately activated against self-antigens (Chen & Flies, 2013, Nature Reviews Immunology). Therapeutic interventions like checkpoint inhibitors (e.g., Nivolumab) and costimulation blockers (e.g., Abatacept) target specific proteins within this interaction to modulate immune activity. Because the term encompasses entire cell populations and numerous distinct signaling pathways, it is not classified as a discrete therapeutic target in drug discovery.
Modulation of the immunological synapse through the targeting of costimulatory or coinhibitory signaling pathways to regulate T cell priming and effector function.
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