Copyright
©The Author(s) 2022.
World J Gastroenterol. Jan 28, 2022; 28(4): 479-496
Published online Jan 28, 2022. doi: 10.3748/wjg.v28.i4.479
Published online Jan 28, 2022. doi: 10.3748/wjg.v28.i4.479
Figure 3 Fibrinogen-like protein 2 expression was robustly inducted upon proinflammatory macrophage activation.
A: Flow cytometry of fibrinogen-like protein 2 (Fgl2) +KCs expressing iNOS and CD206 under homeostatic conditions (left), and frequency of iNOS+ and CD206+ cells subsets (right); B: Representative image of Fgl2+MoMFs expressing Ly6C (left), and relative expression level of Fgl2 in Ly6ChiMoMFs and Ly6Clo MoMFs under physiological conditions (right); C: Time course-presentation of Fgl2 expression in M1 polarized KCs (left), and expression level of Fgl2 in Ly6ChiMoMFs and Ly6Clow MoMFs, respectively (right); D: Cell counts of Fgl2+ MoMFs (left), and relative level of Fgl2 expression on both MoMFs subset (right) following viral infection. Data are presented as mean ± SD (n = 5). These experiments were repeated at least three times. MFI: Mean fluorescence intensity.
- Citation: Xiao F, Wang HW, Hu JJ, Tao R, Weng XX, Wang P, Wu D, Wang XJ, Yan WM, Xi D, Luo XP, Wan XY, Ning Q. Fibrinogen-like protein 2 deficiency inhibits virus-induced fulminant hepatitis through abrogating inflammatory macrophage activation. World J Gastroenterol 2022; 28(4): 479-496
- URL: https://www.wjgnet.com/1007-9327/full/v28/i4/479.htm
- DOI: https://dx.doi.org/10.3748/wjg.v28.i4.479