Regulation of pulmonary fibrosis by chemokine receptor CXCR3
J. Clin. Invest. Dianhua Jiang, et al. 114:291 doi:10.1172/JCI16861 [Go to this article.]

Figure 3
NK and NK T cell deficiency in CXCR3^–/– mice. FACS analysis of NK cells from lung, liver, and peripheral blood using specific Ab to the NK cell marker, NK1.1, and T cell markers CD3 or αβTCR. (A) Single cell homogenates from unchallenged lungs of WT C57BL/6 and CXCR3^–/– mice were stained with NK1.1 and anti-CD3e and were subject to flow-cytometric analysis. Analysis was performed on lymphocyte-gated events. The percentages of NK1.1⁺CD3^– or NK1.1⁺CD3⁺ populations are indicated. Four animals in each group were tested. Similar results were obtained in four separate experiments. (B) FACS analysis of NK and NKT cells from liver. The percentage of NK1.1⁺CD3^– or NK1.1⁺CD3⁺ populations are indicated. Four animals in each group were tested. Similar results were obtained in three separate experiments. (C) FACS analysis of NK cells from peripheral blood. The percentages of NK1.1⁺αβTCR^– population are indicated. (D) Intracellular staining for IFN-γ. Single-cell homogenates from C57BL/6 mice challenged with bleomycin for 24 hours were stained for cell surface markers NK1.1 and CD3 and for intracellular IFN-γ. After gating on CD3⁺ and NK1.1⁺, the percentage of IFN-γ–producing cells from CD3^–NK1.1⁺ and CD3⁺NK1.1^– populations is shown.