Journal: ImmunoHorizons
Article Title: Lack of pathogenic involvement of CCL4 and its receptor CCR5 in arthritogenic alphavirus disease
doi: 10.1093/immhor/vlaf022
Figure Lengend Snippet: Antibody-mediated CCL4 depletion and administration of recombinant mouse CCL4 failed to alter Mayaro disease severity. C57BL/6J mice were intravenously inoculated with IgG2a isotype or anti-mouse CCL4 mAb (20 µg/mouse) at −1, 1, 3, and 5 dpi (n = 5). For CCL4 cytokine treatment, C57BL/6J mice were treated with PBS or recombinant mouse CCL4 (400 ng/mouse) through the intraperitoneal route at −3, −1, 1, 3, and 5 dpi (n = 5). Mice were inoculated with 10 4 PFU of MAYV in both hind feet after the first dose of CCL4 antibody or the second dose of CCL4 cytokine and monitored for disease development until 7 dpi (A–C). Weight loss (A), footpad swelling (B), and viremia (C) were determined after CCL4 depletion in C57BL/6J mice (D–E). Weight loss (D), footpad swelling (E), and virus replication (F) were measured after CCL4 treatment. Weight loss and footpad swelling were analyzed using multiple unpaired t tests with the Holm-Sidak method for multiple comparisons, and viremia data was analyzed by unpaired t test with Welch’s correction. The error bars represent the standard deviation, the solid line indicates mean values, and the dotted line represents the limit of detection.
Article Snippet: For in vivo CCL4 neutralization, 6- to 8-wk-old C57BL/6J mice were intravenously inoculated through the retro-orbital sinus with 20 μg/mouse of Rat IgG2a kappa isotype control (Cat. No. 50-112-9680, Fisher Scientific) or an anti-mouse CCL4 mAb (Cat. No. PIMA523742, clone 46907, Fisher Scientific) at −1, 1, 3, and 5 dpi, as previously described.
Techniques: Recombinant, Virus, Standard Deviation
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