口腔扁平苔藓浸润细胞免疫组化分析

这探讨免疫应答在扁平苔藓发病过程中的作用及相互关系，本研究中应用ＡＢＣ技术，用Ｔ３、Ｔ４、Ｔ８、ＩｇＧ单抗及Ｓ－１００蛋白标记病损已浸润细胞。结果表明：病损区以细胞免疫为主，淋巴细胞数量与上皮钉突的增殖程度呈正相关；病损区中郎罕氏细胞明显偏高；基低膜区损害与Ｔ细胞数量呈正相关；ＩｇＧ阳性细胞散在分布于病损区，其阳性物质在基底膜区沉积。提示该疾病以细胞免疫为主，同时有体液免疫应答的参与。     

口腔扁平苔藓病损区T细胞亚群数量与其病程、类型关系的研究

本文采用免疫组织化学方法检测了ＯＬＰ病损区Ｔ细胞亚群的分布情况，结果显示，在发病早期ＯＬＰ病损区浸润Ｔ细胞以Ｔｈ细胞为主，而在晚期则以Ｔｅ／ｓ细胞为主。作者认为这种变化与其在ＯＬＰ发病中的作用有关，即Ｔｈ细胞主要在ＯＬＰ发病的早期阶段起作用，而Ｔｅ／ｓ细胞则对病损的持续存在、发展扩大有重要意义。     

再述口腔扁平苔藓细胞免疫学研究进展——关于细胞介导的免疫损伤机理、人类白细胞抗原免疫调节因子的研究

<正> 本文续上篇“口腔扁平苔藓细胞免疫学研究进展,进一步综述近年来关于该病细胞免疫发病机理研究的新动向。一、口腔扁平苔藓(OLP)病变局部细胞介导的免疫性损伤发病机理及证据:主要承担着介导细胞免疫反应的T淋巴细胞亚群在OLP病损局部为主要浸润细胞,其数量、分布及亚群比例在病变局部、病程发展     

口腔扁平苔藓病损区T细胞亚群数量与其病程,类型半系的研究

本文采用免疫组织化学方法检测了ＯＬＰ病损区Ｔ细胞亚群的分布情况，结果显示，在发病早期ＯＬＰ病损区浸润Ｔ细胞以Ｔｈ细胞为主，而在晚期则以Ｔｃ／ｓ细胞为主。作者认为这种变化与其在ＯＬＰ发病中的作用有关。即Ｔｈ细胞主要在ＯＬＰ发病的早期阶段起作用，而Ｔｃ／ｓ细胞则对病损的持续存在、发展扩大有重要意义。     

口腔粘膜扁平苔癣浸润细胞免疫组织化学研究

本文应用抗T细胞亚类的单克隆抗体(McAb)对口腔粘膜扁平苔癣上皮浸润细胞的性质及其分布情况进行研究。发现上皮下浸润细胞主要是由T淋巴细胞组成。总T细胞为57.8％。T_4细胞为38.3％。T_8细胞25.2％。T_(ao)细胞5.2％。在病损的早期主要由辅助—诱导性T细胞和单核——巨噬细胞介导,T_4/T_8比例增高;在病损后期是以抑制——细胞毒性T细胞(T_5/T_c)所介导的免疫反应,T_8细胞增多,T_4/T_8比例下降,并且T_8细胞多靠近基底膜区分布,提示OLP可能是一种由细胞介导的免疫反应。     

复发性阿弗他溃疡细胞免疫发病机制新进展

复发性阿弗他溃疡（RAU）患病率居口腔黏膜病之首，目前病因及致病机制仍不明。近年对RAU的病因研究多集中在免疫学方面，其中又以细胞免疫为主，细胞免疫主要是指T淋巴细胞介导的免疫应答反应。多项研究证明，RAU患者存在细胞免疫功能下降和T淋巴细胞亚群失衡，细胞免疫的识别、激活、效应三个阶段均表现出异常反应。本文就RAU细胞免疫三个阶段异常反应的最新研究进展作一综述。     

口腔扁平苔藓免疫学因素的研究现状

口腔扁平苔藓(OLP)是一种严重影响患者身心健康的发生于口腔黏膜的非传染性炎症性疾病。OLP的病因尚不明确,可能与多种因素有关。目前的研究表明,OLP的发病与免疫因素密切相关,它是一种以T淋巴细胞介导的免疫应答为特征的慢性疾病。抗原特异性机制和非特异性机制可能参与OLP的免疫过程。首先由树突状细胞摄取、处理未知抗原触发其免疫反应,导致T淋巴细胞和其他免疫细胞在病损处聚集,分泌大量细胞因子,继而破坏基底膜并杀伤角质形成细胞,最终造成口腔黏膜炎症性病损。因此,免疫细胞和复杂的细胞因子网络在OLP的发病过程中起重要作用。本文从免疫机制,免疫细胞和炎症介质三方面对OLP的免疫学研究现状进行综述,旨在为OLP的预防、诊断和临床治疗提供理论参考。     

口腔扁平苔藓的免疫发病机理

口腔扁平苔藓(LP)病损区浸润的主要细胞是T淋巴细胞。T淋巴细胞的两个主要亚群——辅助性/诱导性T细胞(CD_4~+)和抑制性/细胞毒性T细胞(CD_3~+)分别在病变的初期和后期占主要比例.在病损的上皮和结缔组织内均可见到抗原提呈细胞郎格罕细胞(LC)的数量增加和/或激活。细胞介导免疫反应可能是口腔LP的发病机理的关键.     

细胞凋亡相关蛋白Bcl-2对OLP病损区淋巴细胞聚集的影响

目的:探讨凋亡相关蛋白Bcl-2在口腔扁平苔藓(OLP)病变中的生物学行为及对OLP皮损中浸润淋巴细胞聚集、分布的影响,进一步了解OLP的发病机制。方法:采用免疫组织化学检测法,与正常口腔黏膜对照,观察分析25例OLP皮损中Bcl-2蛋白的表达水平及淋巴细胞聚集、分布。结果:OLP病损区T细胞中Bcl-2过度表达,固有层淋巴细胞异常克隆、聚集,浸润增加。结论:OLP病损区中T细胞高密度聚集可能是Bcl-2诱导的局部淋巴细胞过度增殖后关联反应。     

Sioegren综合征涎腺组织T、B淋巴细胞分布的免疫组化研究

Sioegren综合征（SS）涎腺损害机制尚不清楚，作者采用T、B淋巴细胞单克隆抗体，结合ABC技术及图像处理系统检测了21例不同类型SS患者涎腺组织中淋巴细胞亚群分布特征及与浸润细胞关系，发现SS涎腺组织以T细胞为主，与浸润细胞多少无关，提示细胞免疫在局部病变形成中可能具有重要作用。     

The gingival plasma cell infiltrate in HIV-positive patients with periodontitis is disorganized

Patients infected with the human immunodeficiency virus (HIV) are highly susceptible to chronic marginal periodontitis (CMP) and the lesion is generally characterized by abundant plasma cell infiltration. HIV-induced reduction of CD4+ T cells may indirectly affect local production of immunoglobulins (Ig). Gingival biopsies taken from 10 HIV+ and 12 HIV- control patients with CMP were washed, fixed in ethanol and embedded in paraffin. Sections were examined after immunohistochemical staining with monoclonal antibodies against IgA, IgA1-2, IgG, IgG1-4, IgM and IgE. Ig-containing cells were counted in 3 separate connective tissue zones (subjacent to pocket epithelium, central zone and subjacent to oral epithelium). HIV+ patients showed a remarkably increased density of all Ig-containing cells in the connective tissue zone subjacent to the oral epithelium (p<0.05) and a lower % of IgG2+ cells in the entire gingival section (p<0.05). In HIV+ patients, the density of IgG-containing cells in the gingiva was strongly correlated with the serum IgG concentration. The altered topical distribution might imply impaired restriction of the inflammatory lesion, additional antigenic challenges by unusual microorganisms in the oral cavity, or be secondary to HIV-induced dysregulation of the B-cell system.     

Clinical features and mechanistic insights regarding IgG4-related dacryoadenitis and sialoadenitis: a review

Immunoglobulin G4-related disease (IgG4-RD), recognized only recently as a single diagnostic entity, is a chronic inflammatory condition of unknown etiology. The diagnosis of IgG4-RD relies heavily on histopathological analysis and the correlation of histology findings with clinical, serological, and radiological data. CD4⁺ T and B cells, including IgG4-expressing plasmablasts, constitute the major inflammatory cell populations in IgG4-RD and are believed to cause organ damage and tissue fibrosis. Patients with IgG4-RD, who have active, untreated disease, exhibit marked expansion of IgG4-secreting plasmablasts in the blood. Important mechanistic insights correlated with the pathogenesis of IgG4-RD have been disclosed in recent years through the application of novel molecular biology approaches, including next-generation and single-cell RNA sequencing. Exploration of the interactions between these CD4⁺ T cells and cells of the B lymphocyte lineage is critical to understanding the pathophysiology of IgG4-RD. The establishment of pathogenic T cell clones and the identification of antigens specific to these clones constitute the first steps in determining the pathogenesis of this disease. This review focuses on clinical features and mechanistic insights regarding IgG4-related dacryoadenitis and sialoadenitis, from a perspective suitable for oral and maxillofacial surgeons.     

Human T-cell responses to oral streptococci in human PBMC-NOD/SCID mice

We investigated cellular and humoral immune responses to oral biofilm bacteria, including Streptococcus mutans, Streptococcus anginosus, Streptococcus sobrinus, and Streptococcus sanguinis, in NOD/SCID mice immunized with human peripheral blood mononuclear cells (hu-PBMC-NOD/SCID mice) to explore the pathogenicity of each of those organisms in dental and oral inflammatory diseases. hu-PBMC-NOD/SCID mice were immunized by intraperitoneal injections with the whole cells of the streptococci once a week for 3 weeks. FACS analyses were used to determine the percentages of various hu-T cell types, as well as intracellular cytokine production of interleukin-4 and interferon-gamma. Serum IgG and IgM antibody levels in response to the streptococci were also determined by enzyme-linked immunosorbent assay. S. anginosus induced a significant amount of the proinflammatory cytokine interferon-gamma in CD4(+) and CD8(+) T cells in comparison with the other streptococci. However, there was no significant differences between the streptococci in interleukin-4 production by CD4(+) and CD8(+) T cells after inoculation. Further, S. mutans significantly induced human anti-S. mutans IgG, IgG(1), IgG(2), and IgM antibodies in comparison with the other organisms. In conclusion, S. anginosus up-regulated Th1 and Tc1 cells, and S. mutans led to increasing levels of their antibodies, which was associated with the induction of Th2 cells. These results may contribute to a better understanding of human lymphocyte interactions to biofilm bacteria, along with their impact on dental and mucosal inflammatory diseases, as well as endocarditis.     

Immunofluorescence of anti-actin antibody in gingivai epithelium

The presence of actin in migrating oral epithelial cells during wound healing is being studied. Gingival biopsies of rat oral mucosae were taken at sequential postwounding times and primarily incubated in serum containing an anti-actin antibody from either actin-sensitized rabbits or from patients with chronic aggressive hepatitis. Sections were secondarily incubated in fluorescein conjugated goat IgG anti-rabbit or anti-human IgG respectively. Controls employed cryostat sectioned rat intestine incubated with anti-actin antibody as the positive control. The findings from these indirect irnmunofluorescent wound-healing studies demonstrate a sequential increase in detectable epithelial cell actin during migration and maturation.     

CD4~+CD25~+调节性T细胞在口腔鳞状细胞癌中的变化及临床意义

目的 观察CD4+CD25+调节性T细胞特异性转录因子FOXP3在口腔鳞状细胞癌(鳞癌)中的表达情况,以探讨其在口腔鳞癌发生发展中的临床意义。方法 通过免疫组化SP法检测10例正常口腔黏膜组织和36例口腔鳞状细胞癌中FOXP3的表达。结果 FOXP3阳性的CD4+CD25+调节性T细胞在高分化组中的阳性率为26.4%、中分化组为42.7%、低分化组为63.5%,与正常组2.81%相比,差异有统计学意义(P<0.05),且其阳性率与与肿瘤分化程度密切相关(P<0.05)。结论 FOXP3阳性的CD4+CD25+调节性T细胞的表达水平的增加与机体免疫功能低下密切相关,其在口腔鳞癌的发生发展中可能起着重要的作用。     

Immunocompetent cells in periapical granuloma III--quantitative relations of B-lymphocyte sub-population

Our previous studies established that T lymphocytes predominated in diffuse mononuclear infiltrates, whereas B cells were found more frequently in focal infiltrates. In the present study we analysed B cell subpopulation ratios in different types of periapical granuloma mononuclear infiltrates. We used fluorochrome conjugated polyclonal antibodies, specific for human immunoglobulin G, A and M. Quantitative studies showed the presence of B cells with all immunoglobulin classes. The results were as follows: a) the quantitative analysis of cells with different classes of immunoglobulins in diffuse mononuclear infiltrates showed the predominance of IgG (60.65%) in comparison to IgA (24.76%) and IgM (14.59%) positive cells. b) in focal mononuclear infiltrates the prevalence of IgG positive cells was more pronounced (77.15%) comparing to IgA (14.06%) and IgM (8.79%) positive cells (p less than 0.001). Differences in the number of IgA and IgM positive cells did not reach the level of statistical significance. c) the finding of substantial number of B cells, especially of IgG positive cells, suggested that focal infiltrate could be the consequence of exarcerbation of granuloma process caused by delayed action of the agent.     

Possible role of T cells in the establishment of IgG plasma cell-rich periodontal lesion –Augmentation of IgG synthesis in the polyclonal B cell activation response by autoreactive T cells

The effect of T cells on T-independent polyclonal B cell activation (PBA) was studied in vitro in mice. Helper/inducer T cells were activated by interaction with la antigens expressed on B cells. The activated T cells enhanced IgG synthesis in the PBA reaction. la antigen expression on B cells increased when stimulated by polyclonal B cell activators. An autoreactive T cell line was established by longterm culture of spleen cells with polyclonal B cell activators. The culture supernatant from this autoreactive T cell line enhanced IgG synthesis in PBA. The above results suggest that autoreactive T cells were activated by la expressed on B cells stimulated with polyclonal B cell activators, and then prompted B cells to synthesize IgG. Therefore, autoreactive T cells may play an important role in the establishment of the IgG plasma cell-rich periodontal lesion.     

Immunofluorescent detection of actin in non-muscle cells of the developing mouse palatal shelf

Cryostat sections of foetal mouse heads, taken at 14–15 days in utero, were incubated first in serum containing smooth muscle auto-antibody and then in fluorescein-conjugated rabbit or goat IgG directed against human IgG. A positive fluorescent reaction was observed in epithelial and mesenchymal cells of the secondary palate, oral mucosa, nasal septum and tongue. Incubating the auto-antibody-containing serum with highly purified actin blocked the auto-antibody and produced no reaction, suggesting that the contractile protein detected in non-muscle cells of the developing palatal shelf contain the muscle protein, actin.     

Periodontal bone loss and immune characteristics after adoptive transfer of Actinobacillus-sensitized T cells to rats

The immune response, gingival inflammation and periodontal bone loss were examined in rats receiving adoptive transfer of Actinobacillus actinomycetemcomitans (Aa) -sensitized T cells and oral infection with Aa. Thirty-eight, 30-day-old, male Rowett phenotypically normal (rnu/+) heterozygous rats were placed into three groups: 1) Aa -sensitized T cell transfer group ( Aa T), 2) sham-sensitized T cell transfer group (ST) and 3) no transfer control group (C), infected with Aa , and then sacrificed at 120 d of age. Blastogenesis of splenocytes to PHA and Con A was observed in Aa T and ST animals that exceeded the values in C animals. Positive antigenic lymphoproliferation and delayed-type hypersensitivity (foot pad swelling) to Aa were found in Aa T group rats, but weak responses were observed in ST and C group rats. Serum IgG, salivary IgA and IgG antibody concentrations to Aa were elevated in Aa T and ST groups compared with the control group after infection with Aa. The numbers of gingival T and B lymphocytes in the Aa T group were increased in comparison to the other groups. There was also an obvious increase in horizontal bone loss in the Aa T group rats. It is suggested that certain subsets of antigen-specific T cells may augment destructive functions on periodontal tissues.     

PD-L2融合蛋白对角质形成细胞/T细胞共培养模型的作用

目的：探讨人PD-L2融合蛋白对体外模拟口腔扁平苔藓（OLP）局部发病机制的角质形成细胞/T细胞共培养模型的影响。方法：分离培养健康人的角质形成细胞、T细胞,建立共培养模型。实验组加入人PD-L2融合蛋白,阴性对照组加入人IgG1,空白对照组加入含0.1%BSA的PBS,分别继续共培养72h。流式细胞术检测共培养模型中T细胞凋亡及生长周期的改变,MTT法检测T细胞增殖状态,ELISA检测共培养上清中IL-2、IFN-γ表达水平。结果：人PD-L2融合蛋白抑制了共培养模型中T细胞增殖及细胞因子IL-2、IFN-γ的表达,促进了T细胞凋亡,但是对T细胞生长周期没有明显的影响。结论：人PD-L2融合蛋白对体外角质形成细胞/T细胞共培养模型中T细胞增殖活化有一定负性作用,可能是该融合蛋白拮抗了PD-L2与其第二受体配接后促进T细胞增殖的效应,人PD-L2融合蛋白有望成为OLP新的有效的免疫治疗方法。