Is t-cell suppression mediated by mesenchymal stem cells deficient in patients with severe aplastic anemia?
The ability of MSC to downregulate T-cell priming, proliferation, and cytokine release is deficient in patients with SAA, persists indefinitely after immunosuppressive therapy, but seems to be restored after BMT. Whether these abnormalities are relevant to the pathogenesis of aplastic anemia remains to be determined.
These results demonstrate that OP-1 can abrogate the catabolic events associated with a HA6-induced matrix depletion model of osteoarthritis. The mRNA levels of two major cartilage extracellular matrix components, aggrecan and hyaluronan synthase-2 are enhanced above values obtained by either OP-1 or HA6 treatments alone.