[An experimental study on the regulation of bone marrow-derived mesenchymal stem cells through indoleamine 2,3-dioxygenase signaling pathway by thymosin α1 for improving the immunosuppression mediated by T cell].
Hou. Fang F; Huang. Jian-Ming JM; Zhang. Rong R; Li. Lan L; Li. Ge G
Key Findings
- Thymosin‑alpha‑1 lowers TLR9 and raises IDO expression in MSCs in a dose‑ and time‑dependent manner
- MSC cells treated with thymosin‑alpha‑1 inhibit T‑cell proliferation more strongly than untreated MSCs
- The enhanced immunosuppression is linked to a TLR9‑dependent IDO signaling pathway
Practical Outcomes
- The findings suggest thymosin‑alpha‑1 can boost the immune‑modulating ability of certain stem cells, but because the work is limited to in‑vitro experiments on diseased cells, there’s no actionable dosing or protocol for healthy people. Biohackers should wait for human clinical data before considering thymosin‑alpha‑1 for immune or longevity purposes.
Summary
A lab study showed that the peptide thymosin‑alpha‑1 can change signaling in bone‑marrow stem cells from children with aplastic anemia, making those cells better at suppressing T‑cell activity, but this was done in cell cultures, not in people, so it isn’t a ready‑to‑use protocol for healthy individuals.
Abstract
To study the regulatory effect of thymosin α1 (Tα1) on immunosuppression of bone marrow mesenchymal stem cells (MSCs) from children with aplastic anemia (AA) through Toll-like receptor 9(TLR9)and indoleamine 2,3-dioxygenase (IDO) signaling pathway. Bone marrow T cell subsets from children with AA and normal individuals were measured by using flow cytometry. Expressions of TLR9/IDO mRNA of MSCs cocultured with Tα1 were determined by reverse-transcription PCR (RT-PCR). Inhibition of PHA-activated T cell proliferation and activation by MSCs cocultured with Tα1 was detected by using MTT assay and flow cytometry. CD4(+)/CD8(+) ratio (0.64 ± 0.02) in children with AA was significantly lower than that in normal individuals (1.42 ± 0.05); but CD8(+)/CD38(+) ratio (0.92 ± 0.04) was significantly higher than that in normal individuals (0.65 ± 0.05). AA MSCs obviously expressed TLR9, but not IDO; AA MSCs treated with Tα1 downregulated TLR9 expression but upregulated IDO expression in concentration- and time-dependent manners. The inhibition of AA MSCs on T cell proliferation (21.38% ± 12.34%) was lower than that in normal individuals (62.72% ± 17.79%, P < 0.05), while AA MSCs treated with Tα1 for 18 h exhibited a stronger inhibition (42.83% ± 16.54%, P < 0.05). The immunosuppression mediated by MSCs could be improved by Tα1 through upregulation of IDO expression via TLR9-dependent signaling pathway. This research provides a new idea for targeted immunomodulatory therapy with bone marrow MSCs from children with AA.
Study Information
pubmed
2011