Expression of major histocompatibility complex class II and CD80 by gingival epithelial cells induces activation of CD4+ T cells in response to bacterial challenge
Expression of major histocompatibility complex class II and CD80 by gingival epithelial cells induces activation of CD4+ T cells in response to bacterial challenge
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DOI：
10.1128/iai.73.2.1044-1051.2005
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发表时间：
2005-02-01
影响因子：
3.1
通讯作者：
Taubman, MA
中科院分区：
文献类型：
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作者：
Matsuyama, T;Kawai, T;Taubman, MA
HLA-DR（主要组织相容性复合体[MHC] II类）通常由牙周病牙龈组织的上皮细胞表达，而不是由健康牙龈组织的细胞表达。共聚焦显微镜分析显示，来自牙周病组织的牙龈上皮细胞（GEC）表达HLA-DR和B7-1 （CD80）共刺激分子。建立大鼠GEC系，探讨GEC对MHC H类和B7-1表达的影响。γ干扰素（ifn - γ）刺激大鼠GEC细胞系可诱导MHC II类的表达，而通过逆转录pcr和流式细胞术检测，该细胞系组成性地表达B7-1共刺激分子。放线菌comitans omp29特异性CD4(+) Th1克隆细胞对固定A.放线菌comitans和ifn - γ预处理GEC有增殖反应。然而，Th1细胞对单独使用细菌或单独使用ifn - γ的GEC预处理没有反应。MHC H类抗体或CTLA4免疫球蛋白（CTLA4- ig）可抑制GEC诱导的Th1克隆细胞的活化。尽管在ifn - γ处理过的GEC中培养的淋巴结T细胞和Th1克隆细胞对葡萄球菌肠毒素A的超抗原活性敏感，但淋巴结T细胞对放线菌comitans没有超抗原活性。这些结果表明，GEC可以通过MHC II类结合B7共刺激，吸收细菌抗原，加工并将细菌抗原呈递到CD4(+) T细胞。GEC似乎通过刺激抗原特异性CD4(+) T细胞在适应性免疫应答中发挥作用。
HLA-DR (major histocompatibility complex [MHC] class II) is often expressed by epithelial cells in gingival tissues with periodontal disease but not by cells in healthy gingival tissues. Confocal microscopic analyses revealed that gingival epithelial cells (GEC) from tissue with periodontal disease express both HLA-DR and B7-1 (CD80) costimulatory molecules. Rat GEC lines were established to elucidate the possible role of MHC class H and B7-1 expression by GEC. Stimulation of a rat GEC line with gamma interferon (IFN-gamma) induced the expression of MHC class II, whereas the cell line constitutively expressed B7-1 costimulatory molecules as determined by reverse transcription-PCR and flow cytometry. Actinobacillus actinomycetemcomitans Omp29-specific CD4(+) Th1 clone cells proliferated in response to pretreatment of GEC with fixed A. actinomycetemcomitans and IFN-gamma. However, the Th1 cells did not respond to pretreatment of GEC with the bacteria alone or IFN-gamma alone. The activation of Th1 clone cells induced by the GEC was inhibited by antibody to MHC class H or by CTLA4 immunoglobulin (CTLA4-Ig). Lymph node T cells did not demonstrate superantigen activity to A. actinomycetemcomitans, although both lymph node T cells and Th1 clone cells were sensitive to superantigen activity of staphylococcal enterotoxin A as cultured in the presence of IFN-gamma-treated GEC. These results suggested that GEC can take up bacterial antigen and consequently process and present the bacterial antigen to CD4(+) T cells by MHC class II in conjunction with B7 costimulation. GEC appeared to play a role in the adaptive immune response by stimulating antigen-specific CD4(+) T cells.