Figure 4
Figure 4. NY1DD mice have increased pulmonary lymphocyte expression of CXCR3 and increased whole lung expression of IFN-γ and IFN-γ–inducible chemokines. (A) Representative flow cytometry plots of CXCR3 expression on pulmonary lymphocytes from C57BL/6, NY1DD, NY1DD treated with goat serum, and NY1DD treated with goat anti-CXCR3 serum. (B) Pulmonary lymphocytes from NY1DD mice express significantly increased levels of CXCR3 compared with C57BL/6 mice. NY1DD animals treated with anti-CXCR3 display significantly decreased expression of CXCR3 on pulmonary lymphocytes. (C-D) Pulmonary homogenates from NY1DD animals have significantly increased levels of IFN-γ and IFN-γ–inducible chemokines (CXCL9 and CXCL10). NY1DD animals treated with anti-CXCR3 have significantly elevated levels of IFN-γ–inducible chemokines (CXCL9 and CXCL10). Data were analyzed by one-way ANOVA with Neuman-Keuls posttesting (*P < .05).

NY1DD mice have increased pulmonary lymphocyte expression of CXCR3 and increased whole lung expression of IFN-γ and IFN-γ–inducible chemokines. (A) Representative flow cytometry plots of CXCR3 expression on pulmonary lymphocytes from C57BL/6, NY1DD, NY1DD treated with goat serum, and NY1DD treated with goat anti-CXCR3 serum. (B) Pulmonary lymphocytes from NY1DD mice express significantly increased levels of CXCR3 compared with C57BL/6 mice. NY1DD animals treated with anti-CXCR3 display significantly decreased expression of CXCR3 on pulmonary lymphocytes. (C-D) Pulmonary homogenates from NY1DD animals have significantly increased levels of IFN-γ and IFN-γ–inducible chemokines (CXCL9 and CXCL10). NY1DD animals treated with anti-CXCR3 have significantly elevated levels of IFN-γ–inducible chemokines (CXCL9 and CXCL10). Data were analyzed by one-way ANOVA with Neuman-Keuls posttesting (*P < .05).

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