Cell homing

Cell homing is a complex, multi-step physiological process by which circulating cells, such as hematopoietic stem cells, leukocytes, and mesenchymal stem cells, actively migrate to and colonize specific anatomical niches or sites of tissue injury [2, 3]. This process is governed by a coordinated molecular cascade involving the initial tethering and rolling of cells on the vascular endothelium (mediated by selectins), activation through chemokine signaling (notably the CXCR4/CXCL12 axis), and firm adhesion followed by extravasation (mediated by integrins like VLA-4 or α4β7) [4, 13]. While essential for physiological immune surveillance and regenerative medicine, dysregulated cell homing is a primary driver of disease progression in conditions such as cancer metastasis and chronic inflammation [2, 8]. In drug development, specific components of the homing machinery are targeted by agents like Plerixafor (a CXCR4 antagonist) or Vedolizumab (an integrin inhibitor) to either prevent pathological cell infiltration or enhance the delivery of cell-based therapies like CAR-T or stem cells [6, 12]. Because 'cell homing' describes a biological mechanism rather than a single molecular entity, it is classified as a process rather than a discrete therapeutic target receptor or enzyme [3, 11].

Other names

Cellular homingLeukocyte homingStem cell homingLymphocyte traffickingTissue-specific recruitment

Modulation of cell recruitment to specific tissues by targeting adhesion molecules (e.g., integrins, selectins) or chemokine signaling pathways (e.g., CXCR4/CXCL12 axis) to either block pathological infiltration or promote therapeutic localization.