Skip to main content
. 2022 May 12;5:449. doi: 10.1038/s42003-022-03376-y

Fig. 1. Ncf1 deficiency sensitized mice to the effects of β-glucan without enhancing clinical arthritis in CAIA.

Fig. 1

Arthritis severity (a), prevalence (b) was assessed in mice exposed to CAIA initiated by i.v. anti-collagen type II antibodies (aCol2 ab) and triggered by i.p. 1,3–1,6-β-glucan on day 5 to compare Ncf1-deficient (Ncf1*/*) mice and wild-type mice with MN + mice having functional Ncf1 expressed under human CD68 promoter. The mice and the spleens were weighted at euthanasia day after β-glucan in combination with aCol2 ab, and spleen indexes calculated to correlate the spleen weight with the bodyweight of the mouse in CAIA (c). Mice and the spleens were weighed also after intraperitoneal β-glucan exposure. Representative images of splenomegaly are shown in (d). Bodyweight, spleen weight, and the spleen index are shown in (e). The bodyweight curves of mice exposed to CAIA initiated by i.v. anti-collagen type II antibodies (aCol2 ab) and triggered by i.p. 1,3–1,6-β-glucan on day 5 is shown in (f, g). Data are pooled from two experiments in (a, b and f, g); data in (c and e) are pooled from several experiments. Statistical analyses were performed by Mann–Whitney test. *P < 0.05; **P < 0.01; and ***P < 0.001. Results are presented as mean ± SEM.