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. Author manuscript; available in PMC: 2021 Oct 1.
Published in final edited form as: J Thromb Haemost. 2020 Aug 19;18(10):2468–2481. doi: 10.1111/jth.15014

Figure 2. Schematic representation of the role of Plg-RKT in innate immunity.

Figure 2.

Plg-RKT receptor is required for macrophage and lymphocyte recruitment to inflammatory sites. (A) Mechanistically, this effect is mediated by plasmin(ogen) binding and activation via Plg-RKT, by the release of the monocyte chemoattractant CCL2 and by activation of the matrix metalloproteinases pro-MMP2 and pro-MMP-9. (B) Plg-RKT receptor increases the release of IL-6 and IL-10 cytokines. (C) Plg-RKT is preferentially expressed on M1-like macrophages, while during inflammation Plg-RKT decreases CD86 expression. In a similar way, Plg-RKT promotes expression of macrophage M2 markers and (D) enhances efferocytosis of apoptotic cells (4). This diagram has not been published previously.