Immunomodulation via cytokine secretion by mesenchymal stem cells

Immunomodulation via cytokine secretion by mesenchymal stem cells (MSCs)" does not refer to a single, well-defined molecular target such as a receptor, enzyme, or transporter. Instead, it describes a broad cellular process in which MSCs modulate immune responses primarily through the **secretion of cytokines and growth factors**. These secreted factors include **IL-6, IL-10, TGF-β, VEGF, PGE2, chemokines (e.g., CCL-2, CCL-5)**, and others, which together alter the activity of a wide variety of immune cells—T and B lymphocytes, macrophages, dendritic cells, NK cells, and more[1][2][3]. MSCs can suppress pro-inflammatory responses (e.g., reducing Th1, Th17, and cytotoxic T cell activity), induce regulatory T cells, promote the anti-inflammatory M2 phenotype in macrophages, and inhibit B cell maturation and antibody production[2][3][6]. These effects are mediated by both **direct cell contact** and **paracrine signals**, including the release of extracellular vesicles/exosomes carrying bioactive molecules[4][6]. This immunomodulatory function underpins the therapeutic potential of MSCs in treating inflammatory and immune-mediated diseases—ranging from autoimmune disorders and graft-versus-host disease to myocardial infarction and COVID-19[4][6]. MSC-based products or engineered MSC therapies use these pathways but are not directed at a single molecular target. Because "Immunomodulation via cytokine secretion by MSCs" is **not a discrete molecular target** by standard pharmacological definitions, but rather a cellular mechanism, the entry is considered **incorrect as a target** for structured listings alongside receptors, enzymes, and similar entities[4][6].

Other names

MSC immunomodulationMSC paracrine cytokine effectMesenchymal stem cell cytokine secretionMSC-mediated immune regulation

Paracrine secretion of immunomodulatory cytokines (e.g., IL-6, IL-10, TGF-β, PGE2, VEGF, chemokines) Direct cell-cell contact with immune cells Exosome and extracellular vesicle release Induction of T regulatory cells Suppression of pro-inflammatory immune cell subsets