Fig. 2

Monocyte mSema7A shedding mediated by ADAM17 may be one of the reasons of increased serum sSema7A in KD. a Percentage of Sema7A⁺ monocytes in CD14⁺ cells. The result shown is representative of FCM findings from KD-nCAL (n = 6), KD-CAL (n = 6) and HC (n = 6). b Percentage of Sema7A⁺ cells in CD3⁺ T cells and CD15⁺ granulocytes from KD-nCAL (n = 6), KD-CAL (n = 6) and HC (n = 6). c The relationship between serum sSema7A concentration and monocyte counts in KD (n = 68). d Concentration of sSema7A in the culture supernatant of healthy donor monocytes treated with MMP9, ADAM17 and TAPI-1 (a specific ADAM17 inhibitor). Data are expressed as mean ± standard error of mean (M ± SEM) from 3 separate experiments. e The relationship of sSema7A with ADAM17 and MMP9 in the sera of KD patients (n = 68). *P < 0.05; **P < 0.01; n.s.: not significant. Sema7A: Semaphorin 7A; HC: health control; KD: Kawasaki disease; CAL: coronary artery lesions; nCAL: no CAL; MMP9: matrix metalloproteinase 9; ADAM17: A disintegrin and metalloproteinase domain 17