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Fig. 1 | Journal of Translational Medicine

Fig. 1

From: Cellular and molecular mediators of lymphangiogenesis in inflammatory bowel disease

Fig. 1

Cellular mediation of lymphangiogenesis. Both immune cells and non-immune cells play a role in the complex process of inflammatory-associated lymphangiogenesis in vitro and in vitro. LECs express chemotactic molecules that promote macrophage infiltration. In turn, macrophages secrete paracrine prolymphangiogenic growth factors such as VEGF-C, VEGF-D, and VEGF-A in response to inflammatory stimuli. Neutrophils conduce to lymphangiogenesis primarily by modulating VEGF-A bioavailability and bioactivity, and to a lesser extent, secreting VEGF-D. However, the suppressive mechanism of lymphangiogenesis by platelets might further contribute to persistent inflammation. cDCs produce VEGF-C when stimulated by IFN-γ released from NK cells during co-cultured with activated NK cells. In turn, VEGF-C reduces the secretion of IFN-γ from NK cells

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