title: Emerging functions of amphiregulin in orchestrating immunity, inflammation, and tissue repair.
abstract: Type 2 inflammatory responses can be elicited by diverse stimuli, including toxins, venoms, allergens, and infectious agents, and play critical roles in resistance and tolerance associated with infection, wound healing, tissue repair, and tumor development. Emerging data suggest that in addition to characteristic type 2-associated cytokines, the epidermal growth factor (EGF)-like molecule Amphiregulin (AREG) might be a critical component of type 2-mediated resistance and tolerance. Notably, numerous studies demonstrate that in addition to the established role of epithelial- and mesenchymal-derived AREG, multiple leukocyte populations including mast cells, basophils, group 2 innate lymphoid cells (ILC2s), and a subset of tissue-resident regulatory CD4(+) T cells can express AREG. In this review, we discuss recent advances in our understanding of the AREG-EGF receptor pathway and its involvement in infection and inflammation and propose a model for the function of this pathway in the context of resistance and tissue tolerance.
authors.affiliation: Ashworth Laboratories, Institute of Immunology and Infection Research, University of Edinburgh, Edinburgh, EH9 3FL, UK. Electronic address: dietmar.zaiss@ed.ac.uk.
authors.forename: Dietmar M W
authors.initials: DMW
authors.lastname: Zaiss
authors.affiliation: Department of Medicine, Center for Immunity and Inflammation, Rutgers, The State University of New Jersey, New Jersey Medical School, Newark, NJ 07101, USA. Electronic address: gausewc@njms.rutgers.edu.
authors.forename: William C
authors.initials: WC
authors.lastname: Gause
authors.affiliation: Jill Roberts Institute for Research in IBD, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medical College, Cornell University, New York, NY 10021, USA.
authors.forename: Lisa C
authors.initials: LC
authors.lastname: Osborne
authors.affiliation: Jill Roberts Institute for Research in IBD, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medical College, Cornell University, New York, NY 10021, USA. Electronic address: dartis@med.cornell.edu.
authors.forename: David
authors.initials: D
authors.lastname: Artis
mesh_terms: D066258:Amphiregulin; D000818:Animals; D066255:EGF Family of Proteins / Q000276:immunology*; D066246:ErbB Receptors / Q000276:immunology*; D006373:Helminthiasis / Q000276:immunology; D006801:Humans; D007108:Immune Tolerance / Q000276:immunology*; D007249:Inflammation / Q000276:immunology*; D007251:Influenza, Human / Q000276:immunology; D051379:Mice; D009369:Neoplasms / Q000276:immunology; D009976:Orthomyxoviridae Infections / Q000276:immunology; D012038:Regeneration; D019139:Tumor Escape / Q000276:immunology; D014945:Wound Healing / Q000276:immunology*
chemical_list: C587848:AREG protein, human; D066258:Amphiregulin; C587849:Areg protein, mouse; D066255:EGF Family of Proteins; D066246:ErbB Receptors