a, Schematic of the exon/intron structures of the Y64G10A.6 (ilcr-1), F56D1.2 (ilcr-2), and T22H6.1 (ilc-17.1) genes, with the location of mutations used in assays indicated. The terms -1 FS and -7 FS denote frameshift mutations with 1 and 7 base pair deletions. Other alleles are shown in Extended Data Table 1. b, Schematic showing the bordering and aggregation assay. The number of animals on the edge of the food lawn, or in groups, was counted 24 h after animals were transferred to the assay plates. c, Bordering and aggregation phenotypes of single-, double-, and triple-null mutants of ilc-17.1, ilcr-1, and ilcr-2; n = 4 assays; ***P < 0.001, ANOVA with Tukey correction. d, CRISPR induced mutations in the F56D1.2 (ilcr-2) gene, and the F25D1.3 and C44B12.6 genes, which show homology to mammalian IL-17. e, Bordering and aggregation assays for the F25D1.3 and C44B12.6 mutants; n = 4 assays. NS, not significant (ANOVA with Tukey correction). f, Alignment of the SEFIR domains of IL-17 receptors, including C. elegans ILCR-1 and ILCR-2. g, Alignment of IL-17D proteins with ILC-17.1. Arrowheads indicate conserved cysteine residues. h, ILC-17.1 forms disulfide-linked dimers. SDS–PAGE of affinity-purified Flag–ILC-17.1 boiled in sample buffer with or without 100 mM DTT. i, The O2 response defects of ilc-17.1 and ilcr-1 mutants are rescued by Mos1-mediated single copy insertion (MosSCI) of ilc-17.1 and ilcr-1 transgenes; n = 4 assays, 120 animals. ***P < 0.001, Mann–Whitney U-test. j, The O2 response defects of ilc-17.1, ilcr-1, and nfki-1 double mutants with the natural npr-1 215F allele; n = 4 assays, 120 animals. ***P < 0.001, Mann–Whitney U-test.