title: The 3 major types of innate and adaptive cell-mediated effector immunity.
abstract: The immune system has tailored its effector functions to optimally respond to distinct species of microbes. Based on emerging knowledge on the different effector T-cell and innate lymphoid cell (ILC) lineages, it is clear that the innate and adaptive immune systems converge into 3 major kinds of cell-mediated effector immunity, which we propose to categorize as type 1, type 2, and type 3. Type 1 immunity consists of T-bet(+) IFN-γ-producing group 1 ILCs (ILC1 and natural killer cells), CD8(+) cytotoxic T cells (TC1), and CD4(+) TH1 cells, which protect against intracellular microbes through activation of mononuclear phagocytes. Type 2 immunity consists of GATA-3(+) ILC2s, TC2 cells, and TH2 cells producing IL-4, IL-5, and IL-13, which induce mast cell, basophil, and eosinophil activation, as well as IgE antibody production, thus protecting against helminthes and venoms. Type 3 immunity is mediated by retinoic acid-related orphan receptor γt(+) ILC3s, TC17 cells, and TH17 cells producing IL-17, IL-22, or both, which activate mononuclear phagocytes but also recruit neutrophils and induce epithelial antimicrobial responses, thus protecting against extracellular bacteria and fungi. On the other hand, type 1 and 3 immunity mediate autoimmune diseases, whereas type 2 responses can cause allergic diseases.
authors.affiliation: Department of Experimental and Clinical Medicine and the DENOTHE Center, University of Florence, Florence, Italy.
authors.forename: Francesco
authors.initials: F
authors.lastname: Annunziato
authors.affiliation: Innate Immunity, Deutsches Rheuma Forschungszentrum, Berlin, Germany.
authors.forename: Chiara
authors.initials: C
authors.lastname: Romagnani
authors.affiliation: Department of Experimental and Clinical Medicine and the DENOTHE Center, University of Florence, Florence, Italy. Electronic address: sergio.romagnani@unifi.it.
authors.forename: Sergio
authors.initials: S
authors.lastname: Romagnani
mesh_terms: D056704:Adaptive Immunity; D015551:Autoimmunity / Q000235:genetics; D001491:Basophils / Q000276:immunology / Q000473:pathology; D015415:Biomarkers / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology; D003141:Communicable Diseases / Q000235:genetics / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D016207:Cytokines / Q000276:immunology; D004804:Eosinophils / Q000276:immunology / Q000473:pathology; D015870:Gene Expression; D006801:Humans; D006967:Hypersensitivity / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D007111:Immunity, Cellular; D007113:Immunity, Innate; D008407:Mast Cells / Q000276:immunology / Q000473:pathology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology / Q000473:pathology; D058504:Th17 Cells / Q000276:immunology / Q000473:pathology; D018418:Th2 Cells / Q000276:immunology / Q000473:pathology
chemical_list: D015415:Biomarkers; D016207:Cytokines
keywords: T(C)1; T(C)17/T(C)22; T(C)2; T(H)1; T(H)17/T(H)22; T(H)2; Type 1 immunity; innate lymphoid cells; type 2 immunity; type 3 immunity