MS Patient After Stem Cell Therapy
Numerous animal studies support the immunomodulatory activities of stem cells, especially mesenchymal stem cells. For example, expression of molecules such as IDO, IL-10 and TGF-beta by mesenchymal stem cells allows induction of tolerance, generation of Treg cells, as well as veto-like activity. Although there are clinical trials of mesenchymal stem cells in places such as Cambridge University, patients with MS sometimes go to clinics where such therapy is available as a fee for service. Although the cells have established safety profile, their efficacy is not established since Phase III trials have not been performed. The video above is of a patient treated by www.cellmedicine.com describing her experiences.
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Steven Lake said...
J Immunol. 2007 Jul 15;179(2):1322-30. Prevalence of newly generated naive regulatory T cells (Treg) is critical for Treg suppressive function and determines Treg dysfunction in multiple sclerosis.Haas J, Fritzsching B, Trübswetter P, Korporal M, Milkova L, Fritz B, Vobis D, Krammer PH, Suri-Payer E, Wildemann B.
Division of Molecular Neuroimmunology, Department of Neurology, University of Heidelberg, Heidelberg, Germany.
The suppressive function of regulatory T cells (T(reg)) is impaired in multiple sclerosis (MS) patients. The mechanism underlying the T(reg) functional defect is unknown. T(reg) mature in the thymus and the majority of cells circulating in the periphery rapidly adopt a memory phenotype. Because our own previous findings suggest that the thymic output of T cells is impaired in MS, we hypothesized that an altered T(reg) generation may contribute to the suppressive deficiency. We therefore determined the role of T(reg) that enter the circulation as recent thymic emigrants (RTE) and, unlike their CD45RO memory counterparts, express CD31 as typical surface marker. We show that the numbers of CD31-coexpressing CD4CD25CD45RACD45ROFOXP3 T(reg) (RTE-T(reg)) within peripheral blood decline with age and are significantly reduced in MS patients. The reduced de novo generation of RTE-T(reg) is compensated by higher proportions of memory T(reg), resulting in a stable cell count of the total T(reg) population. Depletion of CD31 cells from T(reg) diminishes the suppressive capacity of donor but not patient T(reg) and neutralizes the difference in inhibitory potencies between the two groups. Overall, there was a clear correlation between T(reg)-mediated suppression and the prevalence of RTE-T(reg), indicating that CD31-expressing naive T(reg) contribute to the functional properties of the entire T(reg) population. Furthermore, patient-derived T(reg), but not healthy T(reg), exhibit a contracted TCR Vbeta repertoire. These observations suggest that a shift in the homeostatic composition of T(reg) subsets related to a reduced thymic-dependent de novo generation of RTE-T(reg) with a compensatory expansion of memory T(reg) may contribute to the T(reg) defect associated with MS.
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troopermission said...
The stem cell clinic Cellmedicine appears to be very prolific in terms of scientific papers that their scientists and doctors are publishing, as well as their youtube videos on the channel CELLMEDICINE.
I think that it is going to be more important in the future to continue explaining the immune modulatory abilities of stem cells for the treatment of autoimmunity. Do you have any idea how ignorant people are to the numerous experiments demonstrating that stem cells are capable of not only inhibiting non-specific inflammation but in some situations can cause activation of T regulatory cells that only block pathological autoimmunity?