Journal: Frontiers in Immunology

Article Title: Antagonizing FcαR1 (CD89) as treatment in IgA-mediated chronic inflammation and autoimmunity

doi: 10.3389/fimmu.2023.1118539

Figure Lengend Snippet: Anti-CD89 mAb 10E7 reduces neutrophil influx in a mouse model for linear IgA bullous disease. (A) Injection schedule of mice; Human IgA x human CD89 transgenic mice were injected 7 times with anti-mouse COLXVII human IgA in the right and PBS in the left ears. Treatment with anti-CD89 mAb clone 10E7 or the isotype mouse IgG1 control was given at day 7 and 11. (B) Neutrophil influx in PBS-injected ears (left panels) or human IgA anti-mouse COLXVII- injected ears (right panels) of human IgA x human CD89 transgenic mice that had been treated with anti-CD89 mAb 10E7 (upper panels) or isotype control (lower panels). Dapi (blue (in magnification) or grey (for overview ear)), GR-1 (green). (C) Quantification of neutrophil influx in ears. Mean ± SD are shown. Black circles and black squares represent number of neutrophils in PBS injected or anti-mouse collagen XVII human IgA injected ears of individual mice respectively. Mann-Whitney U tests,*; P<0.05, NS; not significant, mAb; monoclonal antibody, LABD; linear IgA bullous disease, COL; collagen, PBS; phosphate buffered saline, SD; standard deviation.

Article Snippet: Transgenic mice expressing human CD89 and knock-in for human IgA were subcutaneously (sc) injected with 10 μl (7mg/ml) human-anti-mouse Collagen XVII IgA (auto)antibodies (Amsterdam UMC and Polpharma Biologics Utrecht) in the right ear and 10 μl PBS in the left ear as control.

Techniques: Injection, Transgenic Assay, Control, MANN-WHITNEY, Saline, Standard Deviation