Gross, O. et al. Card9 controls a non-TLR signalling pathway for innate anti-fungal immunity. Nature 442, 651–656 (2006).
Jia, X. M. et al. CARD9 mediates Dectin-1-induced ERK activation by linking Ras-GRF1 to H-Ras for antifungal immunity. J. Exp. Med. 211, 2307–2321 (2014).
Glocker, E. O. et al. A homozygous CARD9 mutation in a family with susceptibility to fungal infections. N. Engl. J. Med. 361, 1727–1735 (2009).
Lanternier, F. et al. Deep dermatophytosis and inherited CARD9 deficiency. N. Engl. J. Med. 369, 1704–1714 (2013).
Rosentul, D. C. et al. Genetic variation in the dectin-1/CARD9 recognition pathway and susceptibility to candidemia. J. Infect. Dis. 204, 1138–1145 (2011).
Rosentul, D. C. et al. Gene polymorphisms in pattern recognition receptors and susceptibility to idiopathic recurrent vulvovaginal candidiasis. Front. Microbiol. 5, 483 (2014).
Venselaar, H., Te Beek, T. A., Kuipers, R. K., Hekkelman, M. L. & Vriend, G. Protein structure analysis of mutations causing inheritable diseases. An e-Science approach with life scientist friendly interfaces. BMC Bioinformatics 11, 548 (2010).
Bertin, J. et al. CARD9 is a novel caspase recruitment domain-containing protein that interacts with BCL10/CLAP and activates NF-κB. J. Biol. Chem. 275, 41082–41086 (2000).
Ramensky, V., Bork, P. & Sunyaev, S. Human non-synonymous SNPs: server and survey. Nucleic Acids Res. 30, 3894–3900 (2002).
Franke, A. et al. Genome-wide meta-analysis increases to 71 the number of confirmed Crohn’s disease susceptibility loci. Nat. Genet. 42, 1118–1125 (2010).
McGovern, D. P. et al. Genome-wide association identifies multiple ulcerative colitis susceptibility loci. Nat. Genet. 42, 332–337 (2010).
Janse, M. et al. Three ulcerative colitis susceptibility loci are associated with primary sclerosing cholangitis and indicate a role for IL2, REL, and CARD9. Hepatology 53, 1977–1985 (2011).
Burghardt, K. M. et al. A CARD9 polymorphism is associated with decreased likelihood of persistent conjugated hyperbilirubinemia in intestinal failure. PLoS One 9, e85915 (2014).
Rivas, M. A. et al. Deep resequencing of GWAS loci identifies independent rare variants associated with inflammatory bowel disease. Nat. Genet. 43, 1066–1073 (2011).
Ader, F. et al. Invasive pulmonary aspergillosis in chronic obstructive pulmonary disease: an emerging fungal pathogen. Clin. Microbiol. Infect. 11, 427–429 (2005).
Rivera, A. et al. Dectin-1 diversifies Aspergillus fumigatus-specific T cell responses by inhibiting T helper type 1 CD4 T cell differentiation. J. Exp. Med. 208, 369–381 (2011).
Greenberger, P. A. Allergic bronchopulmonary aspergillosis. J. Allergy Clin. Immunol. 110, 685–692 (2002).
Kauffman, H. F. Immunopathogenesis of allergic bronchopulmonary aspergillosis and airway remodeling. Front. Biosci. 8, e190–e196 (2003).
Knutsen, A. P. et al. Increased sensitivity to IL-4 in cystic fibrosis patients with allergic bronchopulmonary aspergillosis. Allergy 59, 81–87 (2004).
Gavino, C. et al. CARD9 deficiency and spontaneous central nervous system candidiasis: complete clinical remission with GM-CSF therapy. Clin. Infect. Dis. 59, 81–84 (2014).
Steele, C. et al. The β-glucan receptor dectin-1 recognizes specific morphologies of Aspergillus fumigatus. PLoS Pathog. 1, e42 (2005).
Loures, F. V. et al. Recognition of Aspergillus fumigatus hyphae by human plasmacytoid dendritic cells is mediated by dectin-2 and results in formation of extracellular traps. PLoS Pathog. 11, e1004643 (2015).
Fei, M. et al. TNF-α from inflammatory dendritic cells (DCs) regulates lung IL-17A/IL-5 levels and neutrophilia versus eosinophilia during persistent fungal infection. Proc. Natl. Acad. Sci. USA 108, 5360–5365 (2011).
Voehringer, D., Shinkai, K. & Locksley, R. M. Type 2 immunity reflects orchestrated recruitment of cells committed to IL-4 production. Immunity 20, 267–277 (2004).
Gessner, A., Mohrs, K. & Mohrs, M. Mast cells, basophils, and eosinophils acquire constitutive IL-4 and IL-13 transcripts during lineage differentiation that are sufficient for rapid cytokine production. J. Immunol. 174, 1063–1072 (2005).
Hogan, M. B., Piktel, D. & Landreth, K. S. IL-5 production by bone marrow stromal cells: implications for eosinophilia associated with asthma. J. Allergy Clin. Immunol. 106, 329–336 (2000).
Toussaint, M. et al. Host DNA released by NETosis promotes rhinovirus-induced type-2 allergic asthma exacerbation. Nat. Med. 23, 681–691 (2017).
Rivera, A. et al. Innate immune activation and CD4+ T cell priming during respiratory fungal infection. Immunity 25, 665–675 (2006).
Karta, M. R., Broide, D. H. & Doherty, T. A. Insights into group 2 Innate lymphoid cells in human airway disease. Curr. Allergy Asthma Rep. 16, 8 (2016).
Jhingran, A. et al. Tracing conidial fate and measuring host cell antifungal activity using a reporter of microbial viability in the lung. Cell Rep. 2, 1762–1773 (2012).
Hara, H. & Saito, T. CARD9 versus CARMA1 in innate and adaptive immunity. Trends Immunol. 30, 234–242 (2009).
Hailfinger, S. et al. Malt1-dependent RelB cleavage promotes canonical NF-κB activation in lymphocytes and lymphoma cell lines. Proc. Natl. Acad. Sci. USA 108, 14596–14601 (2011).
Chauhan, B., Knutsen, Ap, Hutcheson, P. S., Slavin, R. G. & Bellone, C. J. T cell subsets, epitope mapping, and HLA-restriction in patients with allergic bronchopulmonary aspergillosis. J. Clin. Invest. 97, 2324–2331 (1996).
Chauhan, B. et al. The association of HLA-DR alleles and T cell activation with allergic bronchopulmonary aspergillosis. J. Immunol. 159, 4072–4076 (1997).
Risma, K. A. et al. V75R576 IL-4 receptor alpha is associated with allergic asthma and enhanced IL-4 receptor function. J. Immunol. 169, 1604–1610 (2002).
Brouard, J. et al. Influence of interleukin-10 on Aspergillus fumigatus infection in patients with cystic fibrosis. J. Infect. Dis. 191, 1988–1991 (2005).
Saxena, S., Madan, T., Shah, A., Muralidhar, K. & Sarma, P. U. Association of polymorphisms in the collagen region of SP-A2 with increased levels of total IgE antibodies and eosinophilia in patients with allergic bronchopulmonary aspergillosis. J. Allergy Clin. Immunol. 111, 1001–1007 (2003).
Miller, P. W. et al. Cystic fibrosis transmembrane conductance regulator (CFTR) gene mutations in allergic bronchopulmonary aspergillosis. Am. J. Hum. Genet. 59, 45–51 (1996).
Faccioli, L. H. et al. IL-5 drives eosinophils from bone marrow to blood and tissues in a guinea-pig model of visceral larva migrans syndrome. Mediators Inflamm. 5, 24–31 (1996).
Dubucquoi, S. et al. Interleukin 5 synthesis by eosinophils: association with granules and immunoglobulin-dependent secretion. J. Exp. Med. 179, 703–708 (1994).
Plaut, M. et al. Mast cell lines produce lymphokines in response to cross-linkage of FcεRI or to calcium ionophores. Nature 339, 64–67 (1989).
Takeda, K. et al. Development of eosinophilic airway inflammation and airway hyperresponsiveness in mast cell-deficient mice. J. Exp. Med. 186, 449–454 (1997).
Wilson, S. J., Shute, J. K., Holgate, S. T., Howarth, P. H. & Bradding, P. Localization of interleukin (IL)-4 but not IL-5 to human mast cell secretory granules by immunoelectron microscopy. Clin. Exp. Allergy 30, 493–500 (2000).
Hamelmann, E. et al. Allergen-specific IgE and IL-5 are essential for the development of airway hyperresponsiveness. Am. J. Respir. Cell Mol. Biol. 16, 674–682 (1997).
Robinson, D. S. Mepolizumab for severe eosinophilic asthma. Expert Rev. Respir. Med. 7, 13–17 (2013).
Walsh, G. M. Profile of reslizumab in eosinophilic disease and its potential in the treatment of poorly controlled eosinophilic asthma. Biologics 7, 7–11 (2013).
Ghazi, A., Trikha, A. & Calhoun, W. J. Benralizumab–a humanized mAb to IL-5Rα with enhanced antibody-dependent cell-mediated cytotoxicity–a novel approach for the treatment of asthma. Expert Opin. Biol. Ther. 12, 113–118 (2012).
Stranick, K. S. et al. Identification of transcription factor binding sites important in the regulation of the human interleukin-5 gene. J. Biol. Chem. 272, 16453–16465 (1997).
Mori, A. et al. p38 mitogen-activated protein kinase regulates human T cell IL-5 synthesis. J. Immunol. 163, 4763–4771 (1999).
Bailey, E. et al. FLT3/D835Y mutation knock-in mice display less aggressive disease compared with FLT3/internal tandem duplication (ITD) mice. Proc. Natl. Acad. Sci. USA 110, 21113–21118 (2013).
Yang, H. et al. One-step generation of mice carrying reporter and conditional alleles by CRISPR/Cas-mediated genome engineering. Cell 154, 1370–1379 (2013).
Hsu, Y. M. S. et al. The adaptor protein CARD9 is required for innate immune responses to intracellular pathogens. Nat. Immunol. 8, 198–205 (2007).
Gersuk, G. M., Underhill, D. M., Zhu, L. & Marr, K. A. Dectin-1 and TLRs permit macrophages to distinguish between different Aspergillus fumigatus cellular states. J. Immunol. 176, 3717–3724 (2006).
Zhao, X. et al. JNK1 negatively controls antifungal innate immunity by suppressing CD23 expression. Nat. Med. 23, 337–346 (2017).
Shizuru, J. A., Taylor-Edwards, C., Banks, B. A., Gregory, A. K. & Fathman, C. G. Immunotherapy of the nonobese diabetic mouse: treatment with an antibody to T-helper lymphocytes. Science 240, 659–662 (1988).
Veillette, A., Bookman, M. A., Horak, E. M. & Bolen, J. B. The CD4 and CD8 T cell surface antigens are associated with the internal membrane tyrosine-protein kinase p56lck. Cell 55, 301–308 (1988).
Sauer, K. A., Scholtes, P., Karwot, R. & Finotto, S. Isolation of CD4+ T cells from murine lungs: a method to analyze ongoing immune responses in the lung. Nat. Protoc. 1, 2870–2875 (2006).
Zhao, X. Q. et al. C-type lectin receptor dectin-3 mediates trehalose 6,6′-dimycolate (TDM)-induced Mincle expression through CARD9/Bcl10/MALT1-dependent nuclear factor (NF)-κB activation. J. Biol. Chem. 289, 30052–30062 (2014).