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. 2023 Nov 25;12(23):2707. doi: 10.3390/cells12232707

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© 2023 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Reduction of C5aR2 amplifies STING-induced IFN-β secretion in primary human monocyte-derived macrophages. Non-targeted control (NTC) and C5aR2-edited (C5aR2) primary hMDMs were stimulated with 5 μg/mL STING agonist cAIM(PS)₂ Difluor (Rp/Sp) for 6 h. Supernatants were assessed for (A) IFN-β by ELISA, or (B–G) IL-1β, IL-6, IL-10, TNFα, IL-18 and GM-CSF by Luminex. Mean ± SD, paired Student’s t test. (A) N = 5 independent donors, (B–G) N = 3 independent donors. Fold change between unstimulated and stimulated per genotype was plotted for primary IFN-β to account for donor-to-donor variation in response to agonist. Grey; NTC, Red; C5aR2 edited, light; vehicle, dark; agonist. *: p ≤ 0.05.

Reduction of C5aR2 amplifies STING-induced IFN-β secretion in primary human monocyte-derived macrophages. Non-targeted control (NTC) and C5aR2-edited (C5aR2) primary hMDMs were stimulated with 5 μg/mL STING agonist cAIM(PS)₂ Difluor (Rp/Sp) for 6 h. Supernatants were assessed for (A) IFN-β by ELISA, or (B–G) IL-1β, IL-6, IL-10, TNFα, IL-18 and GM-CSF by Luminex. Mean ± SD, paired Student’s t test. (A) N = 5 independent donors, (B–G) N = 3 independent donors. Fold change between unstimulated and stimulated per genotype was plotted for primary IFN-β to account for donor-to-donor variation in response to agonist. Grey; NTC, Red; C5aR2 edited, light; vehicle, dark; agonist. *: p ≤ 0.05.