title: Th17 cells in type 1 diabetes.
abstract: T1D is an autoimmune disorder, which involves the CD4(+) as well as CD8(+) T-cell-mediated destruction of β cells. Recently, another population of T cells (Th17) is found to be involved in T1D pathology. This review will discuss the characteristics of Th17 cells and the mechanism of Th17-mediated T1D development. Th17 cell expansion is unstrained under T1D condition. Certain Treg cells are defective in T1D and lose the control of Th17 expansion. In addition, the altered function of APCs and a subset of monocytes which spontaneously secrete IL-1β and IL-6 in T1D determine the abnormal expansion of Th17 as well. The pathogenic Th17 cells can cause the imbalance between Teff and Treg cells. Conversion from Th17 to Th1 phenotype and Th17 stimulated CTL responses may play an accessory role in T1D as well. Due to the effects of Th17 on T1D, therapeutic strategies designed to inhibit these cells are applicable and the positive effects are obvious. Taken together, Th17 may exert essential effects on the development of T1D. Identification of the underlying mechanism may inspire new viewpoints for the therapy of this disease.
authors.affiliation: Division of Endocrinology, Tongji Hospital, Tongji Medical College of Huazhong University of Science & Technology, Wuhan, PR China.
authors.forename: Shiying
authors.initials: S
authors.lastname: Shao
authors.forename: Fan
authors.initials: F
authors.lastname: He
authors.forename: Yan
authors.initials: Y
authors.lastname: Yang
authors.forename: Gang
authors.initials: G
authors.lastname: Yuan
authors.forename: Muxun
authors.initials: M
authors.lastname: Zhang
authors.forename: Xuefeng
authors.initials: X
authors.lastname: Yu
mesh_terms: D000818:Animals; D017951:Antigen Presentation; D001324:Autoantigens / Q000276:immunology; D002455:Cell Division; D003602:Cytotoxicity, Immunologic; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000276:immunology; D003922:Diabetes Mellitus, Type 1 / Q000188:drug therapy / Q000276:immunology* / Q000473:pathology; D004195:Disease Models, Animal; D006801:Humans; D020381:Interleukin-17 / Q000037:antagonists & inhibitors / Q000627:therapeutic use; D053583:Interleukin-1beta / Q000378:metabolism; D053759:Interleukin-23 / Q000008:administration & dosage / Q000633:toxicity; D015850:Interleukin-6 / Q000378:metabolism; D007515:Islets of Langerhans / Q000276:immunology / Q000473:pathology; D038041:Lymphopoiesis; D051379:Mice; D016688:Mice, Inbred NOD; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000502:physiology; D050796:STAT3 Transcription Factor / Q000502:physiology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000473:pathology; D058504:Th17 Cells / Q000276:immunology*; D014611:Vaccination
chemical_list: D001324:Autoantigens; C486701:IL25 protein, human; C508600:IL6 protein, human; D020381:Interleukin-17; D053583:Interleukin-1beta; D053759:Interleukin-23; D015850:Interleukin-6; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; C539900:RORC protein, human; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human