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. 2010 Oct 8;25(5):922–931. doi: 10.1016/j.bbi.2010.10.002

Fig. 1.

Fig. 1

Induction of the lymphoid chemokine, CXCL13, is sustained in the brains of mice with SV encephalitis and is produced mainly by microglial cells in vivo. ELISA assays show that a related lymphoid chemokine, CXCL12, is not up-regulated in the brains of SV-infected compared to sham-inoculated mice (not significant (NS) by two-way ANOVA) (A). CXCL13 levels, however, increase and are sustained over the course of acute infection compared to controls (p < 0.0001 by two-way ANOVA) (B). A non-lymphoid chemokine previously implicated in CNS B cell recruitment, CXCL9, is not induced (NS by two-way ANOVA) (C), while another non-lymphoid chemokine previously implicated in this process, CXCL10, is quickly induced but not sustained in CNS tissue (p < 0.0001 by two-way ANOVA) (D). Quantitative PCR analysis of RNA extracted from FACS-sorted CNS cell populations shows that CXCL13 mRNA is found mostly in CD45dim/CD11b+ (microglial) cells, and to a lesser extent in CD45high/CD11b+ (infiltrating myeloid) cells following SV infection (E). Primary microglial cells produce CXCL13 following direct exposure to SV in vitro, while astrocytes do not respond in a similar manner (∗p < 0.05 by Student’s t-test) (F). All bars represent the mean ± SEM of concentrations measured from at least triplicate samples.