Fig. 5: MyD88 and TRIF are required for nonopsonic uptake of C. neoformans without affecting MSR1 expression.

a Wildtype and b Tlr4^−/− macrophages were treated with inhibitors of MyD88, IKKβ (a kinase downstream of MyD88 that is necessary for NF-κB activation), TRIF, and TBK1 (a kinase downstream of TRIF that phosphorylates and activates IRF3) (n = 6 per condition). Following pre-treatment with the various inhibitors, cells were infected with non-opsonised C. neoformans. Data are pooled from two independent experiments. c Immortalised BMDMs from wildtype, Tlr4^−/−, MyD88^−/− and Trif^−/− macrophages were infected with non-opsonised C. neoformans (n = 3). Data is representative of three independent experiments. Phagocytosis was quantified as the number of internalised cryptococcus within 100 macrophages. Data is mean ± SEM and analysed using one-way ANOVA followed by Tukey’s post-hoc test. P-values are shown above each graph. d Baseline surface expression of Macrophage Scavenger Receptor 1 (MSR1) (also known as CD204) was measured in wildtype, Tlr4^−/−, MyD88^−/− and Trif^−/− macrophages using anti-mouse CD204-PE antibody. PE-labelled rat IgG2a κ was used as an isotype control. Receptor expression was measured using flow cytometry and analysed using the FlowJo software. Data is representative of two independent experiments. Percentages refer to the percentage of MSR1-positive cells. Source data are provided as a Source Data file.