Antigen presentation by interferon‐γ‐treated thyroid follicular cells inhibits interleukin‐2 (IL‐2) and supports IL‐4 production by B7‐dependent human T cells
Antigen presentation by interferon‐γ‐treated thyroid follicular cells inhibits interleukin‐2 (IL‐2) and supports IL‐4 production by B7‐dependent human T cells
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干扰素 γ 处理的甲状腺滤泡细胞的抗原呈递可抑制白细胞介素 2 (IL-2)，并支持 B7 依赖性人类 T 细胞产生 IL-4
DOI：
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发表时间：
1997
期刊：
影响因子：
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通讯作者：
R. Lechler
中科院分区：
文献类型：
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作者：
G. Lombardi;K. Arnold;J. Uren;F. Marelli;R. Hargreaves;N. Imami;A. Weetman;R. Lechler
在炎症过程中，抗原对抗原呈递细胞的识别被诱导表达主要组织相容性复合体（MHC） II类分子，其结果尚不清楚。在这项研究中，我们研究了上皮细胞抗原呈递的结果，并使用甲状腺滤泡细胞（TFC）作为模型，这些细胞已知在自身免疫性甲状腺疾病中表达MHC II类分子，并获得向浸润甲状腺的T细胞呈递自身抗原的能力。结果表明，使用来自三个HLA -错配应答者的CD4+ T细胞，表达MHC II类的TFC不能刺激原代T细胞同种异体反应。表型分析显示，经干扰素γ孵育后，TFC不表达共刺激分子B7‐1 （CD80）和‐2 （CD86）。将表达人B7‐1的小鼠DAP.3细胞（DAP.3‐B7）添加到含有外周血CD4+ T细胞和表达DR1‐TFC的培养物中，可导致增殖反应，这表明TFC未能刺激原发性同种异体反应是由于缺乏共刺激。同样，依赖于B7共刺激的受HLA - DR限制的流感特异性T细胞克隆对TFC呈递的肽没有反应；同样，TFC与DAP.3 - B7共培养可以克服缺乏反应。此外，TFC上的抗原识别抑制了B7依赖性T细胞中白细胞介素- 2 （IL - 2）的产生。相反，在辅助T型0 (Th0) T细胞中，IL - 4的释放不受TFC呈递的影响。此外，相对于B7独立的Th0克隆产生IL - 2， TFC抗原呈递更有利于IL - 4的产生。这些结果表明，MHC II类+ TFC抗原呈递可能诱导自身反应性Th1细胞的耐受性，但同时可能促进非承诺T细胞的Th2反应，从而支持自身抗体的产生。
The consequence of recognition of antigen on antigen‐presenting cells that are induced to express major histocompatibility complex (MHC) class II molecules following an inflammatory process is still not clear. In this study, we have investigated the outcome of antigen presentation by epithelial cells and we have used as a model thyroid follicular cells (TFC) that are known to express MHC class II molecules in autoimmune thyroid diseases and acquire the capacity to present autoantigens to T cells infiltrating the thyroid gland. The result show that MHC class II‐expressing TFC were unable to stimulate a primary T cell alloresponse, using CD4+ T cells from three HLA‐mismatched responders. Phenotypic analysis showed that TFC, after incubation with interferon‐γ, do not express the co‐stimulatory molecules B7‐1 (CD80) and ‐2 (CD86). Addition of murine DAP.3 cells expressing human B7‐1 (DAP.3‐B7) to cultures containing peripheral blood CD4+ T cells and DR1‐expressing TFC led to a proliferative response, suggesting that the failure of TFC to stimulate a primary alloresponse was due to a lack of co‐stimulation. Similarly, HLA‐DR‐restricted, influenza‐specific T cell clones dependent on B7 for co‐stimulation did not respond to peptide presented by TFC; again the lack of response could be overcome by co‐culture of TFC with DAP.3‐B7. Furthermore, recognition of antigen on TFC inhibited interleukin‐2 (IL‐2) production in the B7‐dependent T cells. In contrast, in T helper type 0 (Th0) T cells, IL‐4 release was not affected by TFC presentation. In addition, antigen presentation by TFC favored IL‐4 production relative to IL‐2 production by B7‐indpendent Th0 clones. These results suggest that antigen presentation by MHC class II+ TFC may induce tolerance in autoreactive Th1 cells but may simultaneously favors a Th2 response in uncommitted T cells, and thereby support autoantibody production.
佛波酯对同种抗原呈递的影响。
DOI：
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发表时间：
1987
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
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作者：
Minami,M;Ebner,SA;Stadecker,MJ;Dorf,ME
通讯作者：
Dorf,ME