Fig. 2: The alarmin ___domain of IL-33 induces TLSs in PDAC and chemical colitis.
From: IL-33-activated ILC2s induce tertiary lymphoid structures in pancreatic cancer
a, Haematoxylin and eosin staining (H&E) (top) and quantification of intratumoural TLSs (bottom left) and intracolonic lymphoid aggregates (LA; bottom right) in anti-LTβR-treated PDAC (left) and DSS-colitis (right) WT and Il33−/− mice. b, H&E (top) and immunofluorescence (IF; middle) staining, and the TLS density (H&E quantified; bottom) in vehicle (veh.) and rIL-33-treated PDAC mice. PDAC 1–6, orthotopic PDAC mice established with six PDAC cell lines. c,d, Intratumoural TLS maturation states (immunofluorescence quantified) (c), and the B cell frequency and clonality and somatic hypermutation (d) in vehicle-treated and rIL-33-treated PDAC mice. e, H&E and colonic LA quantification in vehicle-treated and rIL-33-treated DSS-colitis mice. Data were collected 2 weeks (a, left), 3 weeks (b, PDAC 3 and 4; c and d) and 3–5 weeks (b, PDAC 1, 2, 5 and 6) after tumour implantation, and 2 weeks after DSS initiation (a (right) and e), pooled from ≥2 independent experiments with n ≥ 2 mice per group with consistent results. n represents the number of individual tumours or organs from individual mice analysed separately, or B cell clones (d, right). The dotted lines in a, b and e show putative TLS/LA; the horizontal bars in a–e show the median. P values were calculated using two-way analysis of variance (ANOVA) with Tukey’s multiple-comparison test (a) and two-tailed Mann–Whitney U-test (b–e). Scale bars, 20 μm (a, b (top) and e) and 10 μm (b (bottom)).
