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Fig. 5 | Arthritis Research & Therapy

Fig. 5

From: Expansion and activation of monocytic-myeloid-derived suppressor cell via STAT3/arginase-I signaling in patients with ankylosing spondylitis

Fig. 5

Inhibition of pSTAT3- arginase-I signaling abrogates the suppressive activity of AS-derived M-MDSCs. a Inhibition of siSTAT3 signaling on M-MDSCs by scramble or siSTAT3 appropriately decreased the level of pSTAT3 (*P < 0.05). b Inhibition of STAT3 signaling on M-MDSCs by Stattic (10 μM) appropriately decreased the level of pSTAT3. Intracellular level of ARG1 is decreased with two independent methods of STAT3 signaling inhibition, including siSTAT3 (c) and Stattic (d). y axis shows MFI (*P < 0.05). ARG1 activity of ankylosing spondylitis patients derived M-MDSCs after pSTAT3 inhibition with siSTAT3 (e) and Stattic (f). Inhibition of STAT3 signaling ablates the suppressive activity of M-MDSCs from ankylosing spondylitis patients. Both pSTAT3 small molecule inhibitor (Stattic) (g), and STAT3 siRNA (h) were able to block the functional suppressive capability of ankylosing spondylitis patients derived M-MDSCs. *P < 0.05; **P < 0.01, compared with controls by unpaired t test ARG1 arginase-I, M-MDSCs monocytic myeloid-derived suppressor cells, pSTAT phosphorylated signal transducer and activator of transcription 3

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Arthritis Research & Therapy

ISSN: 1478-6362

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