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Early‐Onset and Adult Periodontitis Associated With Abnormal Cytokine Production by Activated T Lymphocytes
Author(s) -
Sigusch B.,
Klinger G.,
Glockmann E.,
Simon H.U.
Publication year - 1998
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.1998.69.10.1098
Subject(s) - peripheral blood mononuclear cell , cytokine , immunology , periodontitis , immune system , granulocyte macrophage colony stimulating factor , stimulation , medicine , pathogenesis , granulocyte , endocrinology , biology , in vitro , biochemistry
T here is growing evidence for an important role of the immune system in the pathogenesis of periodontitis. To further characterize the possible immunoregulatory dysfunction of peripheral blood mononuclear cells (PBMC) in periodontitis patients, we investigated functional aspects of PBMC from patients with early‐onset periodontitis (EOP) and adult periodontitis (AP). Compared to controls, we observed decreased proliferative responses of PBMC from patients with EOP following stimulation with a mitogenic stimulus (phytohemagglutinin). To investigate whether this abnormality reflects a modulation in cytokine production, we measured the in vitro production of interleukin (IL)‐3, IL‐5, granulocyte macrophage colony‐stimulating factor (GM‐CSF), and interferon‐γ (IFN‐γ) by activated PBMC. PBMC in EOP patients expressed significantly decreased levels of IFN‐γ protein in response to mitogenic stimulation. Reduced IFN‐γ secretion was associated with decreased IFN‐γ and IL‐2 mRNA expression in these cells, as well as decreased HLA‐DR surface expression on monocytes. On the other hand, we observed significantly higher levels of IL‐5 and GM‐CSF in the same system using PBMC from AP patients. These were comparable to the levels observed for patients with allergic asthma. These data imply that EOP is associated with decreased Th1‐like cytokine expression, and that the PBMC response from patients with AP is predominantly Th2/Th0 in nature. J Periodontol 1998;69:1098–1104 .

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