%0 Journal Article
%T Mesenchymal stem cells in autoimmune diseases: hype or hope?
%A Hans U Scherer
%A Melissa van Pel
%A Ren¨¦ EM Toes
%J Arthritis Research & Therapy
%D 2010
%I BioMed Central
%R 10.1186/ar3036
%X Mesenchymal stem cells (MSCs) are multipotent progenitor cells that can be cultured from various adult and fetal tissues and that are capable of differentiating into multiple mesenchymal lineages including bone, cartilage, tendon, marrow stroma and adipose tissue [1]. Because of their unique regenerative potential, MSCs are considered a promising therapeutic modality for tissue regeneration and repair. Moreover, MSCs are thought to be critically involved in the formation of survival niches for memory T cells and B cells in the bone marrow, thereby regulating the size, stability and plasticity of immunological memory.Awareness has additionally been raised by the finding that MSCs display immunomodulatory properties in vitro, as evidenced by their ability to inhibit T-cell proliferation. This inhibition affects the proliferation of T cells induced by alloantigens, mitogens and CD3-ligation. More over, MSCs have also been shown to inhibit the proliferation of B cells, and possibly the activity of natural killer cells. The molecular interactions responsible for these inhibitory effects observed in vitro are the subject of intense investigations and include the action of prostaglandin E2, nitric oxide, indoleamine 2,3-dioxygenase and programmed death ligand-1 [2].Because of their potent inhibitory effects in vitro, MSCs have been used in several preclinical disease models, most often aiming to inhibit alloreactive immunity such as is observed in graft-versus-host disease (GVHD), and in transplantation models. Several studies have now shown that infusions of MSCs can be effective in controlling GVHD or in promoting engraftment and survival of allogeneic bone marrow cells. Opposing observations have also been reported, however, as injection of allogeneic MSCs has been shown to trigger allospecific immune responses in vivo resulting in graft rejection [3]. Therefore it is conceivable that the modulatory effects observed in in vivo transplantation models are not all mediated
%U http://arthritis-research.com/content/12/3/126