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TGF-β downregulates MHC I surface expression through <t>ALK5</t> and Smad3. (A) Representative histogram of MHC I surface expression and relative GMFI of MHC I surface expression on horse MSCs treated with TGF-β with or without an ALK5 inhibitor, <t>SB525334.</t> Data shown are mean +/− SD for n = 6. Superscript letters indicate significant differences between groups, p < 0.0001 by ANOVA. (B) Representative histogram of MHC I surface expression and relative GMFI of MHC I surface expression on equine MSCs treated with TGF-β with or without a selective Smad3 inhibitor, SIS3. Data shown are mean +/− SD for n = 6. Superscript letters indicate significant differences between groups, p < 0.0001 by ANOVA.
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Figure 4. Anti-TGF-β therapies prevent POD1 plasma-induced NK cell dysfunction. Patient POD1 plasma (red) was pre-incubated with an anti-TGF-β monoclonal antibody (mAb) or isolated healthy NK cells were pre-incubated with the TGF-βR1 small molecule inhibitor (smi) <t>SB525334.</t> Box plot of NK cell activating receptor expression and IFNγ production ((A) (%)/(B) (MFI)) normalized to incubation in baseline plasma. Median ± IQR is shown. # p ≤0.1, * p ≤0.05, ** p ≤0.005.
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Figure 4. Anti-TGF-β therapies prevent POD1 plasma-induced NK cell dysfunction. Patient POD1 plasma (red) was pre-incubated with an anti-TGF-β monoclonal antibody (mAb) or isolated healthy NK cells were pre-incubated with the TGF-βR1 small molecule inhibitor (smi) <t>SB525334.</t> Box plot of NK cell activating receptor expression and IFNγ production ((A) (%)/(B) (MFI)) normalized to incubation in baseline plasma. Median ± IQR is shown. # p ≤0.1, * p ≤0.05, ** p ≤0.005.
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alk5 inhibitor sb525334  (Selleck Chemicals)
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Figure 4. Anti-TGF-β therapies prevent POD1 plasma-induced NK cell dysfunction. Patient POD1 plasma (red) was pre-incubated with an anti-TGF-β monoclonal antibody (mAb) or isolated healthy NK cells were pre-incubated with the TGF-βR1 small molecule inhibitor (smi) <t>SB525334.</t> Box plot of NK cell activating receptor expression and IFNγ production ((A) (%)/(B) (MFI)) normalized to incubation in baseline plasma. Median ± IQR is shown. # p ≤0.1, * p ≤0.05, ** p ≤0.005.
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sb525334 as an alk5/tβri inhibitor  (Tocris)
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Figure 4. Anti-TGF-β therapies prevent POD1 plasma-induced NK cell dysfunction. Patient POD1 plasma (red) was pre-incubated with an anti-TGF-β monoclonal antibody (mAb) or isolated healthy NK cells were pre-incubated with the TGF-βR1 small molecule inhibitor (smi) <t>SB525334.</t> Box plot of NK cell activating receptor expression and IFNγ production ((A) (%)/(B) (MFI)) normalized to incubation in baseline plasma. Median ± IQR is shown. # p ≤0.1, * p ≤0.05, ** p ≤0.005.
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TGF-β downregulates MHC I surface expression through ALK5 and Smad3. (A) Representative histogram of MHC I surface expression and relative GMFI of MHC I surface expression on horse MSCs treated with TGF-β with or without an ALK5 inhibitor, SB525334. Data shown are mean +/− SD for n = 6. Superscript letters indicate significant differences between groups, p < 0.0001 by ANOVA. (B) Representative histogram of MHC I surface expression and relative GMFI of MHC I surface expression on equine MSCs treated with TGF-β with or without a selective Smad3 inhibitor, SIS3. Data shown are mean +/− SD for n = 6. Superscript letters indicate significant differences between groups, p < 0.0001 by ANOVA.

Journal: bioRxiv

Article Title: TGF-β downregulates antigen processing and presentation genes and MHC I surface expression through a Smad3-dependent mechanism

doi: 10.1101/2023.01.30.526196

Figure Lengend Snippet: TGF-β downregulates MHC I surface expression through ALK5 and Smad3. (A) Representative histogram of MHC I surface expression and relative GMFI of MHC I surface expression on horse MSCs treated with TGF-β with or without an ALK5 inhibitor, SB525334. Data shown are mean +/− SD for n = 6. Superscript letters indicate significant differences between groups, p < 0.0001 by ANOVA. (B) Representative histogram of MHC I surface expression and relative GMFI of MHC I surface expression on equine MSCs treated with TGF-β with or without a selective Smad3 inhibitor, SIS3. Data shown are mean +/− SD for n = 6. Superscript letters indicate significant differences between groups, p < 0.0001 by ANOVA.

Article Snippet: Media were exchanged after 48 hours with fresh standard media or TGF-β media with or without IFN-g. TGF-βRI (ALK5) inhibitor SB525334 (10 μM; Selleckchem) or SIS3-HCl (10 μM; Selleckchem) were added into the indicated culture media.

Techniques: Expressing

Figure 4. Anti-TGF-β therapies prevent POD1 plasma-induced NK cell dysfunction. Patient POD1 plasma (red) was pre-incubated with an anti-TGF-β monoclonal antibody (mAb) or isolated healthy NK cells were pre-incubated with the TGF-βR1 small molecule inhibitor (smi) SB525334. Box plot of NK cell activating receptor expression and IFNγ production ((A) (%)/(B) (MFI)) normalized to incubation in baseline plasma. Median ± IQR is shown. # p ≤0.1, * p ≤0.05, ** p ≤0.005.

Journal: International journal of molecular sciences

Article Title: Preventing Surgery-Induced NK Cell Dysfunction Using Anti-TGF-β Immunotherapeutics.

doi: 10.3390/ijms232314608

Figure Lengend Snippet: Figure 4. Anti-TGF-β therapies prevent POD1 plasma-induced NK cell dysfunction. Patient POD1 plasma (red) was pre-incubated with an anti-TGF-β monoclonal antibody (mAb) or isolated healthy NK cells were pre-incubated with the TGF-βR1 small molecule inhibitor (smi) SB525334. Box plot of NK cell activating receptor expression and IFNγ production ((A) (%)/(B) (MFI)) normalized to incubation in baseline plasma. Median ± IQR is shown. # p ≤0.1, * p ≤0.05, ** p ≤0.005.

Article Snippet: When indicated, isolated CD56+ cells were incubated with the TGF-β receptor subunit 1 (ALK5) small molecule inhibitor (smi) SB525334 (Selleck Chemicals) (2 μM/well) for 1 h at 37 ◦C prior to adding plasma.

Techniques: Clinical Proteomics, Incubation, Isolation, Expressing