Immune cell receptors and pathways modulated by Mesenchymal Stem Cells

Immune cell receptors and pathways modulated by Mesenchymal Stem Cells (MSCs) refer to a complex set of interactions rather than a single molecular target. MSCs exert potent immunomodulatory effects by interacting with both innate and adaptive immune cells, including T cells, B cells, natural killer (NK) cells, and macrophages [1][2]. These effects are mediated by the secretion of soluble factors such as indoleamine 2,3-dioxygenase (IDO), prostaglandin E2 (PGE2), and transforming growth factor-beta (TGF-beta), which inhibit the proliferation of pro-inflammatory effector cells [3]. Additionally, MSCs utilize direct cell-cell contact mechanisms, such as the PD-1/PD-L1 and Fas/FasL pathways, to induce apoptosis in activated T cells or shift macrophages toward an anti-inflammatory M2 phenotype [4]. These pathways are of significant therapeutic interest for treating inflammatory and autoimmune conditions, most notably graft-versus-host disease (GvHD) and Crohn's disease [5]. However, because this 'target' encompasses a broad range of signaling networks and cellular behaviors, it presents challenges for drug standardization and the prediction of long-term safety outcomes, such as the potential for MSCs to support tumor stroma or cause ectopic calcification [6]. Sources: [1] Wang et al. (2014) Cell Death & Disease; [2] Aggarwal & Pittenger (2005) Blood; [3] Kyurkchiev et al. (2014) World Journal of Stem Cells; [4] Davies et al. (2017) Stem Cell Research & Therapy; [5] Galipeau & Sensébé (2018) Cell Stem Cell; [6] Volarevic et al. (2018) International Journal of Biological Sciences.

Other names

MSC-mediated immunomodulationMesenchymal stem cell immune regulationMSC-immune cell crosstalk

Mesenchymal Stem Cells (MSCs) modulate immune responses through the secretion of paracrine factors such as indoleamine 2,3-dioxygenase (IDO), prostaglandin E2 (PGE2), and transforming growth factor-beta (TGF-beta), as well as through direct cell-to-cell contact via PD-L1 and FasL, which collectively suppress effector T cell activation and promote regulatory T cell (Treg) expansion.