Down-regulation of murine collagen-induced arthritis by a T cell hybridoma.
Down-regulation of murine collagen-induced arthritis by a T cell hybridoma.
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T 细胞杂交瘤下调小鼠胶原诱导的关节炎。
DOI：
10.1159/000163466
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Kresina,TF
中科院分区：
文献类型：
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作者：
Kresina,TF
利用胶原诱导关节炎（CIA）抑制小鼠BW 5147骨髓瘤细胞与脾细胞的体细胞融合产生T细胞杂交瘤细胞系。两种细胞系的细胞表面表型，抗原识别和下调与CIA相关的红斑和水肿的能力。通过直接结合实验确定了细胞株T101N描绘细胞表面表型Lyl+2- L3T4- Thyl+。细胞株T104B1仅表达Thyl +同种异体抗原。筛选研究、体外IL-2生成的测量以及体内I型和II型胶原抗体的抑制表明，杂交瘤细胞在识别多态间质胶原方面不具有同型特异性。注射1 × 105T101N细胞后，CIA的红斑和水肿出现下调，而T104B1细胞未出现下调。T101N细胞给药33天后，CIA小鼠后爪跗区组织病理与CIA小鼠有明显差异。给予T101N细胞的CIA小鼠关节显示与正常关节结构相似的排列关节面，仅残留关节膜。这些数据表明，胶原特异性克隆T细胞系可以调节显示CIA的关节的大体病理和关节结构。
T cell hybridoma cell lines were generated by somatic cell fusion of BW 5147 myeloma cells and splenic cells from mice suppressed for collagen-induced arthritis (CIA). Two cell lines were characterized for their cell surface phenotype, antigen recognition and capacity to down-regulate the erythema and edema associated with CIA. Cell line T101N was determined to portray the cell surface phenotype Lyl+2- L3T4- Thyl+by a direct binding assay. Cell line T104B1 was determined to express only the Thyl + alloantigen. Panning studies, measurement of IL-2 production in vitro and the suppression of antibodies to type I and type II collagen in vivo indicate that the hybridoma cells are not isotype specific in their recognition of the polymorphic interstitial collagens. Down-regulation of the erythema and edema of CIA occurred on injection of 1 × 105T101N cells but not T104B1 cells. Histology of the tarsus region of the hind paw of CIA mice 33 days after the administration of T101N cells showed contrasting histopathology compared to that of CIA mice. The joints of CIA mice given T101N cells showed aligned articular surfaces resembling normal joint structure and only residual pannus. The data indicate that collagen-specific cloned T cell lines can modulate the gross pathology and joint architecture of joints exhibiting CIA.