“…Therefore, angiogenesis may result from the local production of distinct factors, or via cytokine- and cell-mediated responses that increase local concentrations of VEGF. This interplay between cell-mediated immune reactions and the local delivery of TGF-β and VEGF by monocyte/macrophages have resulted in the development of paradigms to explain how angiogenesis and fibrosis are characteristic of chronic inflammatory disease states (Cotran, 1994; Brown et al, 1995; Freeman et al, 1995; Sharma et al, 1996; Inoue et al, 1998; Majno, 1998; Pilmore et al, 1999; Jain et al, 2000, 2002; Ezaki et al, 2001; Kanazawa et al, 2001; Mannon, 2006; Booth and Bishop, 2010). …”