Fig. 2

Semaphorin 7A (Sema7A) expression, and inflammatory cytokine synthesis induced by Sema7A in primary human cells. a Cell surface expression of Sema7A in peripheral blood CD4⁺ and CD14⁺ cells and peripheral blood mononuclear cells (PBMCs) from patients with rheumatoid arthritis (RA) and healthy volunteer donors. Results shown are representative of findings from nine patients with RA and eight healthy volunteer donors. b Expression of messenger RNA (mRNA) for Sema7A in peripheral blood CD4⁺ and CD14⁺ cells. Results shown are from nine patients with RA and eight healthy individuals. N.S. Not significant. c Cytokine production by PBMCs from healthy donors (n = 6 percytokine) after treatment with or without Sema7A (10 ng/ml) for 24 h. Supernatants were analyzed for expression of IL-17, TNF-α, and IL-6 by enzyme-linked immunosorbent assay. Results are shown as the mean of triplicate values ± SD from one of three representative experiments. *P<0.05 versus unstimulated controls. d Interferon-γ (IFN-γ), IL-17, and IL-22 synthesis by primary human CD4⁺ T cells from patients with RA after treatment with either Sema7A or heat-denatured Sema7A (DSema7A) (both at 10 ng/ml) for 24 h. Data are shown as the mean of triplicate values ± SD as compared with DSema7A (10 ng/ml) or unstimulated CD4⁺ T cells. **P < 0.01. e Tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) production by primary human CD14⁺ monocytes from patients with RA after stimulation with naturally cleaved soluble Sema7A (sSema7A) for 48 h with or without anti-Sema7A antibody. Results shown are representative of three independent experiments