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. 2015 May 4;125(6):2347–2362. doi: 10.1172/JCI80273

Figure 2. STIM1 in T cells controls myeloid cell infiltration of Mtb-infected lungs.

Figure 2

(A) Immunohistochemistry of CD68 expression on monocytes/macrophages in lungs of Mtb-infected mice at 114 d.p.i. Images are representative of 5 mice per group. Original magnification, ×40 (left panels); ×400 (right panels). (B and C) Frequencies of lung myeloid cell populations at 114 d.p.i. Representative flow cytometry plots of 5 mice per group analyzed. Blue gate numbers represent CD11bCD11c+Gr1 AM (no. 1), CD11b+CD11c+Gr1 mDC (no. 2), CD11b+CD11cGr1hi neutrophils (no. 3), CD11b+CD11cGr1int monocytes (no. 4), and CD11b+CD11cGr1 RIM (no. 5). (D) Absolute numbers of myeloid cell populations in the lungs of WT and Stim1CD4 mice (as defined in B and C) over the course of Mtb infection. Line graphs show mean ± SEM of 5 mice per group and time point. (E) Concentrations of the proinflammatory cytokine IL-1β, myeloid growth factors (GM-CSF, M-CSF), and chemokines (MCP-1/CCL2, MIP-1α/CCL3, RANTES/CCL5) in lung homogenate supernatants from Mtb-infected WT and Stim1CD4 mice analyzed at 107 d.p.i. and 114 d.p.i. by multiplex analysis. Individual values for both days are pooled and indicated by symbols. Bar graphs show the mean of 9 mice (4 on 107 d.p.i. and 5 on 114 d.p.i.) per group. Statistical significance was calculated by Student’s t test. *P < 0.05; **P < 0.01; ***P < 0.001.