Tanaka S, Fakher M, Barbour S E, Schenkein H A, Tew J G
Clinical Research Center for Periodontal Diseases, School of Dentistry, Medical College of Virginia Campus/Virginia Commonwealth University, Richmond, VA 23298-0678, USA.
J Periodontal Res. 2006 Feb;41(1):1-9. doi: 10.1111/j.1600-0765.2005.00829.x.
High levels of serum anti-Actinobacillus actinomycetemcomitans immunoglobulin G (IgG) correlate with reduced extent and severity of periodontal disease and the present study was undertaken to begin testing the hypothesis that proinflammatory cytokines are important in the induction of optimal anti-A. actinomycetemcomitans IgG responses.
Studies with pokeweed mitogen indicate that interleukin-1alpha (IL-1alpha) and IL-1beta are necessary for optimal IgG1 and IgG2 production and that prostaglandin E(2) (PGE(2)) and interferon-gamma (IFN-gamma) selectively promote IgG2, which is a major component of the anti-A. actinomycetemcomitans response in vivo. The pokeweed mitogen results suggest that these proinflammatory cytokines would also be necessary for optimal production of IgG specific for A. actinomycetemcomitans.
Peripheral blood mononuclear cells from A. actinomycetemcomitans-seropositive subjects with localized aggressive periodontitis were stimulated with A. actinomycetemcomitans in immune complexes capable of binding follicular dendritic cells that participate in the induction of recall responses in vivo. Cultures were manipulated with anti-IL-1alpha, anti-IL-1beta, anti-IFN-gamma, anti-IL-12, anti-CD21, indomethacin, and PGE(2). Actinobacillus actinomycetemcomitans specific IgG production was monitored by enzyme-linked immunosorbent assay (ELISA).
Addition of follicular dendritic cells to peripheral blood mononuclear cells cultures resulted in follicular dendritic cell-lymphocyte clusters and increased anti-A. actinomycetemcomitans IgG responses (3-40-fold increases) compared with controls lacking follicular dendritic cells. Anti-IL-1alpha, anti-IL-1beta, anti-IFN-gamma, anti-IL-12, anti-CD21 and indomethacin suppressed anti-A. actinomycetemcomitans IgG production by half or more. PGE(2) restored IgG responses suppressed by indomethacin.
The cytokines IL-1alpha, IL-1beta, IFN-gamma, IL-12, and PGE(2) were all necessary for optimal production of human anti-A. actinomycetemcomitans and the need for proinflammatory cytokines including the T helper 1 (Th1) cytokines is consistent with a response with a significant IgG2 component.
血清抗伴放线放线杆菌免疫球蛋白G（IgG）水平升高与牙周病的范围缩小和严重程度降低相关，本研究旨在开始检验以下假设，即促炎细胞因子在诱导最佳抗伴放线放线杆菌IgG反应中起重要作用。
用商陆有丝分裂原进行的研究表明，白细胞介素-1α（IL-1α）和IL-1β对于最佳IgG1和IgG2产生是必需的，并且前列腺素E2（PGE2）和干扰素-γ（IFN-γ）选择性促进IgG2，而IgG2是体内抗伴放线放线杆菌反应的主要成分。商陆有丝分裂原的结果表明，这些促炎细胞因子对于伴放线放线杆菌特异性IgG的最佳产生也是必需的。
用能够结合参与体内回忆反应诱导的滤泡树突状细胞的免疫复合物中的伴放线放线杆菌刺激来自患有局限性侵袭性牙周炎的伴放线放线杆菌血清阳性受试者的外周血单核细胞。用抗IL-1α、抗IL-1β、抗IFN-γ、抗IL-12、抗CD21、吲哚美辛和PGE2处理培养物。通过酶联免疫吸附测定（ELISA）监测伴放线放线杆菌特异性IgG的产生。
与缺乏滤泡树突状细胞的对照相比，向外周血单核细胞培养物中添加滤泡树突状细胞导致滤泡树突状细胞-淋巴细胞簇形成，并增加抗伴放线放线杆菌IgG反应（增加3至40倍）。抗IL-1α、抗IL-1β、抗IFN-γ、抗IL-12、抗CD21和吲哚美辛将抗伴放线放线杆菌IgG产生抑制一半或更多。PGE2恢复了被吲哚美辛抑制的IgG反应。
细胞因子IL-1α、IL-1β、IFN-γ、IL-12和PGE2对于人抗伴放线放线杆菌的最佳产生都是必需的，并且对包括辅助性T细胞1（Th1）细胞因子在内的促炎细胞因子的需求与具有显著IgG2成分的反应一致。
