Chemokine-mediated recruitment of NK cells is a critical host defense mechanism in invasive aspergillosis
J. Clin. Invest. Brad E. Morrison, et al. 112:1862 doi:10.1172/JCI18125 [Go to this article.]

Figure 6
Role of CCR2 in in vivo recruitment of NK cells to the lungs in invasive aspergillosis. CFSE-labeled or unlabeled NK cells from WT or CCR2^–/– animals were transferred to neutrophil-depleted mice before intratracheal challenge with A. fumigatus conidia. Infected mice were treated with PBS or neutralizing anti–MCP-1/CCL2 Ab. (a) Mean ± SEM of number of lung CFSE⁺ CD3^– DX5⁺ NK cells (n = 3–5 mice per group). *P < 0.05 compared with corresponding recipients of WT NK cells. (b) Lung chitin content on day 3 of invasive aspergillosis after NK cell transfer. Mean ± SEM (n = 6 mice per infected groups; n = 2, uninfected group). *P < 0.05 compared with recipients of CCR2^–/– NK cells. (c) Mean ± SEM of number of lung CFSE⁺ CD3^– DX5⁺ NK cells in each group (n = 4–6 mice per group). Anti–MCP-1, mice treated with anti–MCP-1/CCL2 mAb. *P < 0.05 compared with WT recipients of WT NK cells; **P < 0.05 compared with each of the other groups.