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. 2020 Nov 20;11:585134. doi: 10.3389/fimmu.2020.585134

Figure 7.

Figure 7

Blockade of IL-17A and IL-17F is required for optimal inhibition of inflammatory cytokine production by dermal fibroblasts in response to MAIT supernatant. (A) RNAScope staining of KLRB1 (brown) and TRAV1-2 (red) in lesional section from a patient with pustular psoriasis. Co-localization of both probes (black arrows) shows MAIT cells. (B) RNAScope staining of IL-17A and IL-17F in psoriatic lesional skin. IL-17F single producing cells (brown arrows), IL-17A single producing cells (red arrows) and IL-17A+IL-17F+ dual producing cells (black arrows). (C) RNAScope co-localization of KLRB1 with IL-17A or IL-17F in skin sections from two psoriasis patients. (D) Experimental setup to generate MAIT cell supernatant. PBMCs were stimulated with E. coli, IL-12 and Il-18 for 48 h, after which the activated MAIT cells were purified by FACS and cultured for a further 24 h with IL-2, IL-12, and IL-18. (E) Experimental setup to test activity of MAIT cell supernatant in stimulating cytokine release by NHDFs, in the presence or absence of IL-17A and IL-17F neutralization. (F) Cytokine levels in MAIT cell supernatant measured using ‘Th cytokine’ 13-plex LegendPlex. IL-2 is not shown as recombinant IL-2 was included in culture media. (G–I) Cytokines produced by NHDFs supernatants stimulated with MAIT cell supernatant, with or without neutralizing antibodies towards IL-17A, IL-17F, or IL-17A/IL-17F (bimekizumab). One-way ANOVA with Dunnett’s multiple comparisons, shown relative to ‘0’ group. Background cytokine production from unstimulated fibroblasts were subtracted. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.