title: Downregulation of E Protein Activity Augments an ILC2 Differentiation Program in the Thymus.
abstract: Innate lymphoid cells (ILCs) are important regulators in various immune responses. The current paradigm states that all newly made ILCs originate from common lymphoid progenitors in the bone marrow. Id2, an inhibitor of E protein transcription factors, is indispensable for ILC differentiation. Unexpectedly, we found that ectopically expressing Id1 or deleting two E protein genes in the thymus drastically increased ILC2 counts in the thymus and other organs where ILC2 normally reside. Further evidence suggests a thymic origin of these mutant ILC2s. The mutant mice exhibit augmented spontaneous infiltration of eosinophils and heightened responses to papain in the lung and increased ability to expulse the helminth parasite,Nippostrongylus brasiliensisThese results prompt the questions of whether the thymus naturally has the capacity to produce ILC2s and whether E proteins restrain such a potential. The abundance of ILC2s in Id1 transgenic mice also offers a unique opportunity for testing the biological functions of ILC2s.
authors.affiliation: Program in Arthritis and Clinical Immunology, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104.
authors.forename: Hong-Cheng
authors.initials: HC
authors.lastname: Wang
authors.affiliation: Program in Arthritis and Clinical Immunology, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104.
authors.forename: Liangyue
authors.identifier: 0000-0003-0265-1985
authors.initials: L
authors.lastname: Qian
authors.affiliation: Program in Arthritis and Clinical Immunology, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104.
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhao
authors.affiliation: Program in Arthritis and Clinical Immunology, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104.
authors.forename: Joni
authors.initials: J
authors.lastname: Mengarelli
authors.affiliation: Program in Arthritis and Clinical Immunology, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104.
authors.forename: Indra
authors.identifier: 0000-0002-9973-3057
authors.initials: I
authors.lastname: Adrianto
authors.affiliation: Program in Arthritis and Clinical Immunology, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104.
authors.forename: Courtney G
authors.identifier: 0000-0002-9606-3772
authors.initials: CG
authors.lastname: Montgomery
authors.affiliation: Diet, Genomics, and Immunology Laboratory, Beltsville Human Nutrition Research Center, Agricultural Research Service, United States Department of Agriculture, Beltsville, MD 20705; and.
authors.forename: Joseph F
authors.identifier: 0000-0002-1590-8869
authors.initials: JF
authors.lastname: Urban
authors.affiliation: Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104.
authors.forename: Kar-Ming
authors.identifier: 0000-0002-4623-9469
authors.initials: KM
authors.lastname: Fung
authors.affiliation: Program in Arthritis and Clinical Immunology, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104; sunx@omrf.org.
authors.forename: Xiao-Hong
authors.identifier: 0000-0002-7390-7506
authors.initials: XH
authors.lastname: Sun
mesh_terms: D000818:Animals; D002454:Cell Differentiation / Q000276:immunology*; D019070:Cell Lineage / Q000276:immunology; D002469:Cell Separation; D015536:Down-Regulation; D005434:Flow Cytometry; D007113:Immunity, Innate / Q000276:immunology*; D051798:Inhibitor of Differentiation Protein 1 / Q000276:immunology; D008214:Lymphocytes / Q000166:cytology / Q000276:immunology*; D054503:Lymphoid Progenitor Cells / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D008822:Mice, Transgenic; D013950:Thymus Gland / Q000166:cytology / Q000276:immunology*
chemical_list: C497455:Idb1 protein, mouse; D051798:Inhibitor of Differentiation Protein 1