Interleukin‐10 promotes anticollagen antibody production in type I diabetic peripheral B lymphocytes

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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 CDS 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.