Phosphatidylserine receptor (PSR)

Phosphatidylserine (PS) receptors are a diverse group of cell surface proteins, including the TAM (Tyro3, Axl, MerTK) and TIM (TIM-1, TIM-3, TIM-4) families, that recognize PS exposed on the outer leaflet of cell membranes [1][2]. Under physiological conditions, PS exposure is a hallmark of apoptosis, and its recognition by PSRs triggers efferocytosis and the release of anti-inflammatory cytokines like IL-10 and TGF-beta to maintain self-tolerance [1]. In the context of cancer, tumor cells and tumor-associated vasculature often constitutively expose PS, creating an immunosuppressive microenvironment that facilitates tumor growth and immune evasion by activating PSRs on myeloid cells [3]. Therapeutic approaches targeting this pathway include the use of antibodies like bavituximab to block PS-receptor interactions and the development of PS-coated nanoparticles [3][4]. These nanoparticles can either be used to deliver drugs specifically to PSR-expressing cells (like macrophages) or to mimic apoptotic cells to induce immune tolerance in inflammatory and autoimmune diseases [4]. The target name provided in the query is considered incorrect as it combines the biological target (receptors) with a specific delivery modality (nanoparticles). [1] Birge, R. B., et al. (2016). Nature Reviews Cancer. [2] Segawa, K., & Nagata, S. (2015). Annual Review of Immunology. [3] Belzile, O., et al. (2015). Cancer Immunology, Immunotherapy. [4] Shlomovitz, I., et al. (2019). Journal of Controlled Release.

Other names

PS receptorPSTRPhosphatidylserine-binding receptorPhosphatidylserine-recognizing receptorPhosphatidylserine receptors via phosphatidylserine nanoparticle surface

Antagonism of PS-receptor binding to restore anti-tumor immune activity, or agonism via PS-mimetics (such as nanoparticles) to induce anti-inflammatory signaling and immune tolerance.