Fig. 4

Blocking β1-integrin abrogates semaphorin 7A (Sema7A)-induced cytokine production from CD14⁺ cells in rheumatoid arthritis (RA). a Expression of messenger RNA (mRNA) for Sema7A receptors (plexin C1 and β1-integrin) in peripheral blood CD14⁺ cells from patients with RA and from healthy individuals. Results shown are from 14 patients with RA and 12 healthy individuals. Values in a–c are mean ± SEM. *P < 0.05, **P < 0.01. b RA CD14⁺ cells were incubated with the anti-β1-integrin monoclonal antibody (mAb) or anti-plexin C1 mAb in the presence of soluble Sema7A. After 48-h cultivation, supernatants were collected for expression of TNF-α and IL-6 by enzyme-linked immunosorbent assay. Results shown are representative of findings from eight patients with RA and six healthy volunteer donors. c Phosphorylation of focal adhesion kinase (FAK) in THP-1 and CD14⁺ cells upon exposure to Sema7A. Isolated CD14⁺ cells were exposed to 10 ng/ml of recombinant Sema7A. Cells exposed to heat-inactivated Sema7A (DSema7A) were used as negative controls. Phosphorylation of FAK was evaluated by immunoblot analysis. Activation of FAK was detected after 3 min of incubation with Sema7A. Results shown are representative of three independent experiments. NS Not significant