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Immune cell surface receptors mediating exosome uptake are a heterogeneous group of proteins responsible for the recognition and internalization of extracellular vesicles (EVs) by immune cells. This group includes phosphatidylserine receptors like T-cell immunoglobulin and mucin domain-containing protein 4 (TIM-4), sialic acid-binding lectins such as Siglec-1 (CD169), and various integrins like αvβ3 and αLβ2 (LFA-1) (Mulcahy et al., 2014; Saunderson et al., 2014). These receptors facilitate the transfer of bioactive molecules, including proteins, lipids, and nucleic acids, from donor cells to recipient immune cells, thereby modulating immune responses (Miyanishi et al., 2007). In pathological states, particularly cancer, tumor-derived exosomes utilize these receptors to reprogram immune cells into pro-tumorigenic phenotypes, facilitating immune evasion and the establishment of pre-metastatic niches (Hoshino et al., 2015). Therapeutic strategies targeting these receptors aim to block the uptake of pathogenic exosomes to prevent disease progression, though such approaches must carefully balance the inhibition of harmful signaling with the preservation of homeostatic vesicle-mediated communication (Feng et al., 2010).
Blocking the interaction between exosomal ligands and immune cell surface receptors to prevent vesicle internalization and subsequent phenotypic modulation of the recipient cell.
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