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Transcript
Mesenchymal stem cells immunology profiles
Common characteristics
Introduction
- MSCs immunologically privileged
- MSCs inhibiting maturation of T-cells
- MSCs stimulated by pro-inflammatory cytokine (Interferon gamma)
- MSCs can used in immunosuppression and immunomodulation
Immunomodulatory capacity of MSCs
Immunomodulatory capacity of MSCs
- Allogenic cells are deleted by host immune system
- Apart from not being recognised as alloantigens, MSCs are able to suppress the activation and proliferation of different cells of the host immune system
Immunosuppresion
and Immunomodulation
- MSCs inhibit T-cell response to mitogens, antibodies, and allogenic cells.
- T-cells need to be activated before MSCs can trigger response.
- Immunosuppressive properties of MSCs are supposedly triggered by IFNγ
- MSCs can arrest T-cell in G1 growth cycle
Examples:
- Mitogens:- PHA and IL2
- Antibodies:- CD3 and CD28
- Allogenic cells:- PBMCs, Lymphocyte, DCs
Mechanism
MSCs can inhibit T-cell proliferation by cell-to-cell interactions or by releasing several mediators.
Tregs in MSC-Mediated Immunomodulation
- MSCs suppress proliferation of CD4+ and CD8+ lymphocyte in dose dependent and non-specific manner.
- MSCs induce Treg differentiation by enhancing the production of PGE-2, TGF-B and IL-10.
- Treg will produce IFN-γ and IL-10
- IFN-γ and IL-10 will up regulate the suppressor of cytokine signaling 3 (SOCS3) and inhibit STAT3
- MSCs can promote Treg proliferation by suppressing the production of IL-2 and TNF-α via activation of STAT5
- MSCs also activates Treg by increasing the expression of CD39 and CD73.
- These molecules participate in the adenosine-producing pathway required for Tregs to exert their immunosuppressive activities
Th1 in MSC-Mediated Immunomodulation
- Mesenchymal stem cells exert immune suppressive effects through inhibiting Th1 type pro-inflammatory factor expression (such as IFNγ, TNFα and IL1β)
- MSCs promote Th1 cells to secrete the immune suppressor IL10 and thus repress the immune responses
- MSCs also inhibit Th1 cell activation indirectly through suppressing DC and NK cells
Th2 in MSC-Mediated Immunomodulation
- MSCs induce the differentiation and maturation of Th2 cells through IDO expression, which causes tryptophan depletion and tryptophan metabolite production
Th17 in MSC-Mediated Immunomodulation
- MSCs enhance CD54 expression and recruit Th17 cells onto MSCs through CCR6-CCL20
- MSCs could inhibit Th17 differentiation through upregulating PD1, IL10, CCL2 or SOCS3 and inhibiting the STAT3 pathway
- STAT3 pathway inhibition reduces Th17 differentiation through downregulating RORt and IL17 expression
- Th17 inhibition by MSCs also involves PGE2
- The MSCs could even convert the Th17 cells into Treg cells
IDO in MSC-Mediated Immunomodulation
- IDO is the factor released by MSC that can inhibit T-cells
- IDO is a limiting enzyme in trptophan catabolism
- IDO has been related to an increased number of Tregs
Methods
Sample results from FACS
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