Extended Data Fig. 7: LCMV induces influx of migratory cDC1 that express high levels immunostimulatory molecules.

(a–c) Naïve wildtype mice were infected with chronic LCMV-Docile. The spleens and pooled inguinal, brachial, axillary, cervical and mandibular lymph nodes (LN) were harvested on d30 p.i. and enriched for the CD11c⁺MHCII⁺ cells by flow cytometric sorting. The samples were then subjected to scRNA-seq. (a) Normalised expression of myeloid/DC marker genes projected onto the UMAPs. (b) Bubble plot comparing the transcript expression of genes related to DC activation among the main DC subsets obtained from the spleen and LN. (c) Annotated bubble plot showing predicted cell-cell interaction classes between different myeloid/DC subsets (senders) and T_PEX cells (receivers). (d–h) Naïve wildtype mice were infected with chronic LCMV-Docile. The spleens and pooled LN were harvested on d25 p.i., and DC subsets were analysed using flow cytometry. (d) Schematic of the experimental setup. (e) Representative flow cytometry plots and quantification showing the frequencies of CCR7⁺ cells among CD11c⁺MHCII⁺ cells in the spleen and LN on d25 p.i. (n = 13). (f, g) Representative flow cytometry plots and quantification showing the frequencies of migratory DC defined by (f) CD8α^neg (Uninfected: n = 10; LCMV: n = 21) and (g) MHCII^hi (Uninfected: n = 10; LCMV: n = 11) among all LN-derived cDC1 (XCR1⁺) in infected and uninfected mice. (h) Representative flow cytometry plots and (i) quantification showing the expression of MHCII, CD40, CD86, CD80 and IL-12 among splenic and LN cDC1 subsets on d25 p.i. (n = 6). Dots in graphs (e–g, i) represent individual mice; bars represent median. Quantification and statistics derive from two-tailed t tests (e, f) and one-way ANOVA (g, l) and based on all data points across at least two independent experiments.