Fig. 5

ERAP2 induces pyroptosis in RA CD4 + T cells by inhibiting the Hedgehog signaling pathway. CD4⁺ T cells were stimulated for 72 h. Then, normal CD4⁺ T cells were infected with control lentivirus or lentivirus encoding ERAP2 (LV-NC/ LV-ERAP2). RA CD4 + T cells were infected with control shRNA virus or ERAP2 shRNA virus (RA-shcontrol/ RA-shERAP2). A, B SHH, SMO, and GLI1 expression in isolated CD4 + T cells is shown in representative immunoblots (left) and plots of the relative band density for NCs (n = 3) and RA patients (n = 3) with normalization to β-actin expression (right). C, D ERAP2, SHH, SMO, and GLI1 expression in isolated CD4 + T cells with overexpression or knockdown is shown in representative immunoblots (left) and plots of the relative band density with normalization to β-actin expression (right). E, F GLI1, ASC, NLRP3, cleaved Caspase-1 and GSDMD-N expression in isolated CD4 + T cells with GANT58 treatment (20 µm) is shown in representative immunoblots (left) and plots of the relative band density with normalization to β-actin expression (right). G, H GLI1, ASC, NLRP3, cleaved Caspase-1 and GSDMD-N expression in isolated CD4 + T cells with Purmorphamine treatment (20 µm) is shown in representative immunoblots (left) and plots of the relative band density with normalization to β-actin expression (right). All data are shown as the mean ± SD. Statistical significance was determined by one-way ANOVA followed by Bonferroni’s multiple-comparisons test for multigroup comparisons or Student’s t test; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. NC, normal control; RA, rheumatoid arthritis