LOCALIZATION OF TUMOR-NECROSIS-FACTOR-ALPHA IN SYNOVIAL TISSUES AND AT THE CARTILAGE PANNUS JUNCTION IN PATIENTS WITH RHEUMATOID-ARTHRITIS
LOCALIZATION OF TUMOR-NECROSIS-FACTOR-ALPHA IN SYNOVIAL TISSUES AND AT THE CARTILAGE PANNUS JUNCTION IN PATIENTS WITH RHEUMATOID-ARTHRITIS
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DOI：
10.1002/art.1780340908
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发表时间：
1991-09-01
影响因子：
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通讯作者：
MAINI, RN
中科院分区：
文献类型：
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作者：
CHU, CQ;FIELD, M;MAINI, RN
应用免疫亲和纯化的多克隆抗人重组肿瘤坏死因子-α(TNF-α)F(ab‘)2片段和免疫组织化学技术，对类风湿关节炎(RA)和骨性关节炎(OA)患者滑膜组织中产生肿瘤坏死因子-α的细胞进行了定位。11例RA中9例和4例OA中2例有抗肿瘤坏死因子-α抗体阳性细胞，而5例正常滑膜均未见阳性细胞。在RA中，26-%的衬里细胞呈肿瘤坏死因子-α阳性。在聚集间区，10-30%的细胞含有肿瘤坏死因子-α，通常分布在血管周围，淋巴集合体中高达19%的细胞表达肿瘤坏死因子-α。一些内皮细胞也被这些抗体染色。在骨性关节炎组织中，含有肿瘤坏死因子-α的细胞主要分布在深层。在4例RA标本中，软骨-血管膜交界处也可见含肿瘤坏死因子-α的细胞。双重免疫荧光分析显示，RA滑膜中大部分分泌肿瘤坏死因子的细胞表达单核/巨噬细胞标志CD11b和CD14，少数表达T细胞标志CD3。我们的发现提供了组织学证据，表明肿瘤坏死因子-α是由单核/巨噬细胞系的细胞在滑膜衬里和深层局部产生的，支持其在炎症中的作用。此外，我们的研究结果表明，肿瘤坏死因子-α是由软骨-血管膜连接处的细胞产生的，可能会影响软骨细胞的代谢，导致类风湿关节炎的软骨退化。
Using immunoaffinity-purified polyclonal antihuman recombinant tumor necrosis factor-alpha (TNF-alpha) F(ab')2 fragments and immunohistochemical techniques, the cells that make TNF-alpha were localized in the inflamed synovial tissue of patients with rheumatoid arthritis (RA) and osteoarthritis (OA). Anti-TNF-alpha antibody-stained cells were demonstrated in 9 of 11 RA and 2 of 4 OA but none of 5 normal synovial membranes examined. In RA, 26-64% of the lining layer cells were positive for TNF-alpha. In the interaggregate area, 10-30% of the cells contained TNF-alpha, often in a perivascular distribution, and up to 19% of the cells in lymphoid aggregates stained for TNF-alpha. Some endothelial cells also stained with these antibodies. In OA tissues, the TNF-alpha-containing cells were found predominantly in the deeper layer. Cells containing TNF-alpha were also found at the cartilage-pannus junction in all 4 RA specimens examined. Double immunofluorescence analysis demonstrated that most TNF-alpha-secreting cells in the RA synovial membrane expressed the monocyte/macrophage marker antigens CD11b and CD14, and a few expressed the T cell marker CD3. Our findings provide histologic evidence that TNF-alpha is locally produced in the lining and deeper layers of the synovium by cells of the monocyte/macrophage lineage, supporting its role in inflammation. Further, our findings demonstrate that TNF-alpha is produced by cells at the cartilage-pannus junction, which could affect chondrocyte metabolism, leading to the cartilage degradation in RA.