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. Author manuscript; available in PMC: 2021 Apr 7.
Published in final edited form as: J Invest Dermatol. 2018 Dec 27;139(6):1318–1328. doi: 10.1016/j.jid.2018.12.012

Figure 5. MIP-2– and KC-producing skin cells in the first hours of Leishmania major infection.

Figure 5.

Staining for (a) KC and DAPI in naïve and L. major-infected WT and Tlr2−/− mice 4 hours after infection. (b) Staining for MIP-2 and DAPI in WT naïve and infected mice. Magnifications of the indicated area are shown below. The arrows point to MIP-2+ dots presumably showing released chemokine. (c) Noninflamed and inflamed areas of infected WT skin samples stained for MIP-2 and for NIMP-R14highCD11b+ neutrophils. Below is an enlargement of the defined areas. (d) Similar staining as in c performed for naïve and L. major-infected Tlr2−/− mice. (e) Quantification of MIP-2+ cells (arrow head) and dots (small arrow). The number of MIP-2+ events/50,000 μm2 for WT and Tlr2−/− ears is shown ± standard deviation. n = 4 ears/group, representative of two independent experiments. (f) Co-localization of MIP-2 was assessed for CD206+F4/80+ dermal macrophages, CD207/langerin+ Langerhans cells, CD45+ hematopoietic cells, vascular endothelial cadherin+ endothelium, and collagen IV+ endothelium-associated basement membranes. Representative images are shown. Scale bar = 100 μm. ***P < 0.001. c, cartilage; ns, not significant; WT, wild type.