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CD163 is a high-affinity scavenger receptor for hemoglobin-haptoglobin complexes, primarily expressed on the surface of M2-polarized macrophages and monocytes. It plays a critical role in the resolution of inflammation by clearing free hemoglobin and inducing the production of anti-inflammatory cytokines. The combination of "CD163 + β-tubulin" typically refers to a therapeutic strategy involving antibody-drug conjugates (ADCs) where CD163 serves as the cell-surface targeting receptor and a tubulin inhibitor (which targets β-tubulin) serves as the cytotoxic payload. This approach is designed to selectively deplete or reprogram tumor-associated macrophages (TAMs) or inflammatory macrophages, which are often associated with immunosuppression and poor prognosis in cancer and chronic inflammatory diseases. By delivering tubulin-disrupting agents directly to these specific immune cells, researchers aim to modulate the immune microenvironment and enhance anti-tumor or anti-inflammatory responses while minimizing systemic toxicity.
Receptor-mediated endocytosis of the antibody-drug conjugate (ADC) upon binding to CD163, followed by lysosomal degradation and intracellular release of the payload (e.g., tubulin inhibitors like MMAE which bind to β-tubulin to disrupt microtubule polymerization and induce cell death).
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