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Fig. 6 | Molecular Medicine

Fig. 6

From: SIGIRR deficiency contributes to CD4 T cell abnormalities by facilitating the IL1/C/EBPβ/TNF-α signaling axis in rheumatoid arthritis

Fig. 6

Increased TNF-α production led by SIGIRR deficiency was largely abolished by C/EBPβ gene knockdown in primary CD4 T cells treated with IL-1β. Primary CD4 T cells were isolated from wild-type or Sigirr −/− mice spleens and transfected with control or targeting small interfering RNA (siRNA). After 3 days, the primary CD4 T cells were treated with IL-1β for 48 h. The supernatants were collected for ELISA, and the cells were collected for intracellular staining by flow cytometry. A C/EBPβ gene silencing in wild-type mouse primary CD4 T cells 3 days after transfection with control siRNA (scramble siRNA) or C/EBP β-specific siRNA (C/EBPβ siRNA). B Representative FACS plot of intracellular TNF-α expression in wild-type and Sigirr −/− CD4 T cells transfected with scramble or C/EBPβ siRNA. C TNF-α production in the supernatants of wild-type and Sigirr −/− CD4 T cells transfected with scramble or C/EBPβ siRNA. ns, not significant (P > 0.05), *P < 0.05, **P < 0.01 and ***P < 0.001 (unpaired t test, n = 3)

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