title: Interleukin-10 promotes anti-collagen antibody production in type I diabetic peripheral B lymphocytes.
abstract: Previous studies have shown that type I diabetes (IDDM) increases the risk of developing periodontitis by 2-3-fold. IDDM patients exhibit destruction of the pancreatic beta cells, most probably caused by an autoimmune reaction. Evidence is accumulating to support the role of the autoimmune response in periodontal pathogenesis. A cytokine, interleukin (IL)-10, has been reported to selectively promote the expansion of a B lymphocyte lineage (CD5/LY1/B1) which has the propensity for secreting high levels of autoantibody. Therefore, the purpose of this project was to evaluate IL-10 production, percentage of CD5 B cells and the frequency of anti-collagen secreting cells in peripheral blood mononuclear cells of age, gender and race matched IDDM patients and controls. IL-10 production was evaluated by an ELISA using the supernatant of adherent peripheral blood cells cultured for 24 h in the presence of Porphyromonas gingivalis lipopolysaccharide (LPS). In 8 of 31 patients, IL-10 levels were significantly increased in IDDM compared to controls and a higher percentage of CD5 B cells was also observed by flow cytometry. In addition, these patients exhibited a higher frequency of anti-collagen secreting cells as elucidated by an ELISPOT. Moreover, treatment with a neutralizing anti-IL-10 antibody diminished the anti-collagen antibody response by 70%. These findings support the concept that a subset of IDDM patients possess an extremely robust IL-10 response following exposure to Gram-negative LPS, which could predispose them to the development of periodontitis through a heightened autoimmune mechanism.
authors.affiliation: Department of Periodontics, Medical College of Georgia, Augusta 30912-1220, USA.
authors.forename: S H
authors.initials: SH
authors.lastname: Stein
authors.forename: T E
authors.initials: TE
authors.lastname: Hart
authors.forename: W H
authors.initials: WH
authors.lastname: Hoffman
authors.forename: C L
authors.initials: CL
authors.lastname: Hendrix
authors.forename: C J
authors.initials: CJ
authors.lastname: Gustke
authors.forename: S C
authors.initials: SC
authors.lastname: Watson
mesh_terms: D000293:Adolescent; D000328:Adult; D018941:Antigens, CD19; D001323:Autoantibodies / Q000096:biosynthesis*; D001402:B-Lymphocytes / Q000187:drug effects* / Q000378:metabolism; D018956:CD5 Antigens; D016022:Case-Control Studies; D002469:Cell Separation; D002648:Child; D003094:Collagen / Q000276:immunology; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D016130:Immunophenotyping; D016753:Interleukin-10 / Q000096:biosynthesis*; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008070:Lipopolysaccharides / Q000276:immunology; D008213:Lymphocyte Activation; D008297:Male; D010518:Periodontitis / Q000276:immunology*; D016966:Porphyromonas gingivalis / Q000737:chemistry
chemical_list: D018941:Antigens, CD19; D001323:Autoantibodies; D018956:CD5 Antigens; D008070:Lipopolysaccharides; D016753:Interleukin-10; D003094:Collagen