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青少年牙周炎病变中的炎症细胞及其亚群。一项家族研究。

Inflammatory cells and their subsets in lesions of juvenile periodontitis. A family study.

作者信息

Syrjänen S, Markkanen H, Syrjänen K

出版信息

Acta Odontol Scand. 1984 Oct;42(5):285-92. doi: 10.3109/00016358408993882.

Abstract

The inflammatory cells in the gingival biopsy samples from a total of 9 patients with juvenile periodontitis (JP) and from 10 of their family members (JPrelat) belonging to 5 different families were subjected to phenotypic characterization. Plasma cells and their immunoglobulins were stained with immunoperoxidase kits for IgA, IgG, and IgM. B, T, and MPS (cells of the mononuclear phagocyte system) cells were demonstrated by the alpha-naphthyl acetate esterase (ANAE) technique in cryostat sections. The subsets (T helper/inducer and T suppressor/cytotoxic cells) of T cells were detected with monoclonal antibodies OKT4 and OKT8, respectively, using indirect immunofluorescence. Similar studies were completed for 19 age- and sex-matched periodontally healthy subjects. IgG plasma cells for outnumbered the IgA and IgM cells in all three series and were most pronounced in JPrelat series. Most of the inflammatory cells were ANAE-negative (B cells) in all series (78-87%). The highest proportions of T and MPS cells were found in the JP series (10% for both). A statistically significantly higher ratio for TH/Ts (OKT4+/OKT8+) was found in both the JP and JPrelat series as compared with that of the healthy controls. The findings suggest that imbalance (either inherited or acquired) in the immune regulation may play role in the development of JP.

摘要

对来自5个不同家庭的9例青少年牙周炎(JP)患者及其10名家庭成员(JPrelat)的牙龈活检样本中的炎症细胞进行了表型特征分析。用免疫过氧化物酶试剂盒对浆细胞及其免疫球蛋白进行IgA、IgG和IgM染色。在低温切片中,通过α-萘乙酸酯酶(ANAE)技术显示B细胞、T细胞和单核吞噬细胞系统(MPS)细胞。分别使用单克隆抗体OKT4和OKT8,通过间接免疫荧光检测T细胞的亚群(T辅助/诱导细胞和T抑制/细胞毒性细胞)。对19名年龄和性别匹配的牙周健康受试者完成了类似研究。在所有三个系列中,IgG浆细胞的数量均超过IgA和IgM细胞,在JPrelat系列中最为明显。在所有系列中,大多数炎症细胞为ANAE阴性(B细胞)(78%-87%)。在JP系列中发现T细胞和MPS细胞的比例最高(均为10%)。与健康对照组相比,JP和JPrelat系列中TH/Ts(OKT4+/OKT8+)的比例在统计学上显著更高。这些发现表明,免疫调节的失衡(无论是遗传的还是后天获得的)可能在JP的发病机制中起作用。

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