title: Tunicamycin inhibits diabetes.
abstract: BACKGROUND
  Autoimmune diseases are characterized by a breakdown of immunologic tolerance, and this breakdown can lead to life-threatening or lifelong disorders. Moreover; drugs that are used to treat these diseases are few in number and are associated with many serious adverse effects.
  
  
  METHODS
  We used the rat insulin promoter-glycoprotein mouse model to analyze the role of tunicamycin in the process of autoimmune diabetes; the P14 mouse model to analyze the effect of tunicamycin on CD8(+) T cells; chop knockout mice to analyze the role of tunicamycin on an endoplasmic reticulum stress model; and fluorescence-activated cell sorting, quantitative real-time polymerase chain reaction, and histologic methods.
  
  
  RESULTS
  We found that a single dose of tunicamycin reduced the activation and pancreatic infiltration of CD8(+) T cells. This activity delayed the incidence of virus-induced diabetes and improved survival rates.
  
  
  CONCLUSIONS
  Tunicamycin may offer therapeutic opportunities for T cell-mediated autoimmune diseases such as diabetes.
authors.affiliation: Department of Gastroenterology, Hepatology and Infectious diseases, University of Düsseldorf, Germany.
authors.forename: Namir
authors.initials: N
authors.lastname: Shaabani
authors.forename: Nadine
authors.initials: N
authors.lastname: Honke
authors.forename: Philipp A
authors.initials: PA
authors.lastname: Lang
authors.forename: Boris
authors.initials: B
authors.lastname: Görg
authors.forename: Peter
authors.initials: P
authors.lastname: Proksch
authors.forename: Nicole
authors.initials: N
authors.lastname: Gailus
authors.forename: Tomomi
authors.initials: T
authors.lastname: Gotoh
authors.forename: Dieter
authors.initials: D
authors.lastname: Häussinger
authors.forename: Karl S
authors.initials: KS
authors.lastname: Lang
mesh_terms: D000818:Animals; D017209:Apoptosis; D001327:Autoimmune Diseases / Q000188:drug therapy / Q000276:immunology / Q000473:pathology / Q000821:virology; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000187:drug effects*; D049109:Cell Proliferation / Q000187:drug effects; D016207:Cytokines / Q000187:drug effects / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology / Q000821:virology; D059865:Endoplasmic Reticulum Stress; D005434:Flow Cytometry; D006023:Glycoproteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D007166:Immunosuppressive Agents / Q000276:immunology / Q000627:therapeutic use; D008213:Lymphocyte Activation / Q000187:drug effects; D008217:Lymphocytic choriomeningitis virus / Q000737:chemistry / Q000276:immunology / Q000472:pathogenicity; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010179:Pancreas / Q000378:metabolism / Q000473:pathology; D011401:Promoter Regions, Genetic; D051381:Rats; D020133:Reverse Transcriptase Polymerase Chain Reaction; D051742:Transcription Factor CHOP / Q000235:genetics / Q000378:metabolism; D014415:Tunicamycin / Q000627:therapeutic use*
chemical_list: D001786:Blood Glucose; D016207:Cytokines; C497250:Ddit3 protein, mouse; D006023:Glycoproteins; D007004:Hypoglycemic Agents; D007166:Immunosuppressive Agents; D014415:Tunicamycin; D051742:Transcription Factor CHOP