Malignant stem cells (MSCs) can inhibit T cell proliferation in vitro and can therefore be used to treat severe graft-versus-host disease (GVHD).

Studies have shown that when MSCs are cocultured with T cells, indoleamine-pyrrole 2,3-dioxygenase (IDO) is upregulated, leading to tryptophan consumption and the accumulation of its metabolites, thereby reducing T cell proliferation. When natural killer (NK) cells were cultured in the presence of MSCs, activation of the NKp30, NKp44, and NKG2D receptors was suppressed. Sotiropoulou et al.

demonstrated that MSCs inhibit the surface expression of 2B4 and CD132 without affecting CD16 expression in NK cells.

Several other studies have shown that MSCs also participate in immune regulation through paracrine mechanisms.

Guo et al.41 found that after transplantation of MSCs, the expression of TNF-α, IL-1, and IL-6 and apoptosis of cardiomyocytes were significantly reduced, leading to significant improvement in cardiac function in MI rats. Onishi et al. discovered that applying MSCs to a mouse model of MI could reduce the levels of CD68-positive inflammatory cells and monocyte chemotactic protein-1 (MCP-1) in the myocardium, thereby improving cardiac function. Furthermore, MSC-derived conditioned medium could reduce MCP-1-mediated damage to rat cardiomyocytes. Humoral factors produced by bone marrow stromal cells (BMSCs) inhibit the secretion of M antigen-specific immunoglobulin and immunoglobulin G1, thereby inhibiting the terminal differentiation of B cells.