title: Therapeutic Potential of Targeting the Th17/Treg Axis in Autoimmune Disorders.
abstract: A disruption of the crucial balance between regulatory T-cells (Tregs) and Th17-cells was recently implicated in various autoimmune disorders. Tregs are responsible for the maintenance of self-tolerance, thus inhibiting autoimmunity, whereas pro-inflammatory Th17-cells contribute to the induction and propagation of inflammation. Distortion of the Th17/Treg balance favoring the  pro-inflammatory Th17 side is hence suspected to contribute to exacerbation of autoimmune disorders. This review aims to summarize recent data and advances in targeted therapeutic modification of the Th17/Treg-balance, as well as information on the efficacy of candidate therapeutics with respect to the treatment of autoimmune diseases.
authors.affiliation: Department of Rheumatology and Immunology, Medical University of Graz, Auenbruggerplatz 15, 8036 Graz, Austria. patriziafasching@gmx.at.
authors.forename: Patrizia
authors.initials: P
authors.lastname: Fasching
authors.affiliation: Department of Rheumatology and Immunology, Medical University of Graz, Auenbruggerplatz 15, 8036 Graz, Austria. martin.stradner@medunigraz.at.
authors.forename: Martin
authors.initials: M
authors.lastname: Stradner
authors.affiliation: Department of Rheumatology and Immunology, Medical University of Graz, Auenbruggerplatz 15, 8036 Graz, Austria. winfried.graninger@medunigraz.at.
authors.forename: Winfried
authors.initials: W
authors.lastname: Graninger
authors.affiliation: Department of Rheumatology and Immunology, Medical University of Graz, Auenbruggerplatz 15, 8036 Graz, Austria. christian.dejaco@gmx.net.
authors.forename: Christian
authors.initials: C
authors.lastname: Dejaco
authors.affiliation: Department of Rheumatology and Immunology, Medical University of Graz, Auenbruggerplatz 15, 8036 Graz, Austria. johannes_fessler@hotmail.com.
authors.forename: Johannes
authors.initials: J
authors.lastname: Fessler
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D001327:Autoimmune Diseases / Q000188:drug therapy* / Q000235:genetics / Q000276:immunology / Q000473:pathology; D051858:Forkhead Transcription Factors / Q000037:antagonists & inhibitors / Q000235:genetics / Q000276:immunology*; D005786:Gene Expression Regulation; D006801:Humans; D007155:Immunologic Factors / Q000627:therapeutic use*; D007249:Inflammation; D020381:Interleukin-17 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000276:immunology; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000276:immunology*; D010880:Piperidines / Q000627:therapeutic use; D011743:Pyrimidines / Q000627:therapeutic use; D011758:Pyrroles / Q000627:therapeutic use; D015398:Signal Transduction; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D058504:Th17 Cells / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D000069549:Ustekinumab / Q000627:therapeutic use
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D007155:Immunologic Factors; D020381:Interleukin-17; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D010880:Piperidines; D011743:Pyrimidines; D011758:Pyrroles; C539900:RORC protein, human; C568922:sirukumab; C479163:tofacitinib; C555450:secukinumab; D000069549:Ustekinumab
keywords: Foxp3; RORγt; Th17-cells; autoimmunity; regulatory T-cells