Fig. 3: Unc5c plays a role in activation of bone marrow-derived dendritic cells treated with COFs, and in vivo amorphous COF1 accumulate more dendritic cells than crystalline counterpart.
From: Crystallinity of covalent organic frameworks controls immune responses
a–c No significant differences in the percentage of CD86, CD206, and CD163 when mouse DCs treated with COFs with LPS, in the presence of siRNA against Unc5c, in vitro (mean ± s.d, n = 6 biological replicate; one-way ANOVA test). d Associated between upregulation of RIG-I signalling pathway and Unc5c is shown. The RIG-I signalling pathway activates NFkB signalling and induces proinflammatory cytokines. Unc5c modulates microtubule function and vesicle transport in the cytoplasm, then can affect the interaction of DCs with cytotoxic T cells. Biorender file - Acharya, A. (2024) BioRender.com/y57h560. e COFs implanted in the same mouse were analysed for infiltrating innate cells, demonstrate that COF1 recruited higher percentages of dendritic cells and neutrophils as compared to the crystalline COFs, n = 6 mice per group, *p = 0.05–0.01, **p < 0.01, ***p < 0.001.
