The Function of Gingival Lymphocytes on the Establishment of Human Periodontitis
The Function of Gingival Lymphocytes on the Establishment of Human Periodontitis
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牙龈淋巴细胞在人牙周炎形成中的作用
DOI：
10.1177/08959374880020022801
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发表时间：
1988
影响因子：
--
通讯作者：
Y. Harada
中科院分区：
文献类型：
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作者：
H. Okada;Y. Shimabukuro;Y. Kassai;H. Ito;T. Matsuo;S. Ebisu;Y. Harada
人类牙周炎已被证实是一种富含IgG浆细胞的病变。然而，我们也检测到许多T细胞，CD 4阳性和CD 8阳性细胞，在牙周病变。这些T细胞中的一些在其表面上表达HLA-DR（Ia样）抗原，并且HLA-DR+细胞的比例在CD 4+和CD 8+细胞群体中大致相等（Okada et al.，1983年，1984年）。因此，辅助性和抑制性T细胞被认为参与了牙周病变的建立。另一方面，B细胞被认为是多克隆激活牙周病变，因为各种牙周菌群具有多克隆B细胞激活活性。我们证明粘性放线菌T14 V刺激小鼠脾B细胞多克隆，并诱导许多IgM产生细胞，但很少IgG产生细胞。此外，产生IgG的细胞仅从表面IgG阳性B细胞分化而不是从表面IgG阴性B细胞分化，即表面IgM或IgA阳性B细胞（Harada等，1988年）。这些结果表明，记忆B细胞，这已经与适当的抗原引发，可能会迁移到牙周病变，然后被激活的多克隆和发展成为IgG产生细胞。因此，牙周病损可能是由T细胞的免疫调节机制和牙周菌群的多克隆B细胞活性的相互作用引起的。事实上，L3 T4阳性T细胞（辅助诱导T细胞）增强了小鼠脾B细胞的IgG合成，所述小鼠脾B细胞已被T非依赖性B细胞活化剂如LPS和A.粘性制剂（Okada等，1987; Ito等人，1988年）。我们从上述结果推测，自身反应性T细胞识别已用多克隆B细胞活化剂活化的B细胞上增加的自身MHC II（Ia）类抗原，然后产生可溶性因子，其可增强这些B细胞的IgG合成。自身反应性T细胞以及PBAs，因此，可能发挥了重要作用，在建立IgG浆细胞丰富的牙周病变。
Human periodontitis has been confirmed to be an IgG plasma cell-rich lesion. However, we also detected many T cells, both CD4-positive and CD8-positive cells, in periodontal lesions. Some of these T cells expressed HLA-DR (la-like) antigen on their surfaces, and the proportion of HLA-DR+ cells was approximately equal in both CD4+ and CD8+ cell populations (Okada et al., 1983, 1984). Consequently, both helper and suppressor T cells were believed to participate in the establishment of periodontal lesions. On the other hand, B cells were thought to be activated polyclonally in periodontal lesions, because a variety of periodontal florae possessed polyclonal B-cell-activating activity. We demonstrated that Actinomyces viscosus T14V stimulated mouse spleen B cells polyclonally and induced many IgM-producing cells but few IgG-producing cells. Moreover, IgG-producing cells were differentiated from only surface IgG-positive B cells but not from surface IgG-negative B cells-namely, surface IgM- or IgA-positive B cells (Harada et al., 1988). These results suggested that memory B cells, which had already been primed with appropriate antigens, might migrate into periodontal lesions, and then be activated polyclonally and develop into IgG-producing cells. The periodontal lesion could, therefore, be induced by the interactions of immunoregulatory mechanisms of T cells and polyclonal B cell activity of periodontal florae. In fact, L3T4-positive T cells (helper-inducer T cells) enhanced IgG synthesis of mouse spleen B cells which had been activated with T-independent B cell activators such as LPS and A. viscosus preparations (Okada et al., 1987; Ito et al., 1988). We hypothesized from the above results that autoreactive T cells recognized the increasing self-MHC class II(Ia) antigen on B cells which had been activated with polyclonal B cell activators, and then produced soluble factors, which could enhance IgG synthesis of these B cells. Autoreactive T cells as well as PBAs, thus, may play an important role in the establishment of the IgG plasma cell-rich periodontal lesion.