T-lymphocyte surface receptors via MSC adhesion molecules

The target T-lymphocyte surface receptors via MSC adhesion molecules refers to the molecular interface and physical interaction between T-lymphocytes and Mesenchymal Stem Cells (MSCs). This interaction is primarily mediated by specific pairs of cell surface proteins, most notably Intercellular Adhesion Molecule 1 (ICAM-1/CD54) on MSCs binding to Lymphocyte Function-associated Antigen 1 (LFA-1) on T cells, and Vascular Cell Adhesion Molecule 1 (VCAM-1/CD106) on MSCs binding to Very Late Antigen 4 (VLA-4) on T cells (Frontiers in Immunology, 2020). Additionally, the interaction between Activated Leukocyte Cell Adhesion Molecule (ALCAM/CD166) on MSCs and the CD6 receptor on T cells plays a significant role in this interface (World Journal of Gastroenterology, 2025). These adhesion events are critical for the immunomodulatory capacity of MSCs, as they facilitate the close physical proximity required for MSCs to suppress T-cell proliferation and cytokine production through both contact-dependent mechanisms, such as PD-L1/PD-1 signaling, and the localized secretion of suppressive factors like indoleamine 2,3-dioxygenase (IDO) and prostaglandin E2 (PGE2). In clinical practice, components of this interaction are targeted by monoclonal antibodies such as Natalizumab (anti-VLA-4) and Itolizumab (anti-CD6) to treat autoimmune conditions and graft-versus-host disease (GvHD). Understanding this target interface is essential for developing therapies that modulate the immune system's recruitment and activation in inflammatory, autoimmune, and oncological diseases.

Other names

MSC-T cell adhesion interfaceMesenchymal stem cell-T lymphocyte interactionICAM-1/LFA-1 axisVCAM-1/VLA-4 axisALCAM/CD6 axisMSC-mediated immunomodulation complex

Inhibition of T-cell adhesion and migration, disruption of MSC-T cell contact-dependent immunosuppression, and modulation of T-cell activation and proliferation.