UM4D4+ (CDw60) T cells are compartmentalized into psoriatic skin and release lymphokines that induce a keratinocyte phenotype expressed in psoriatic lesions.
UM4D4+ (CDw60) T cells are compartmentalized into psoriatic skin and release lymphokines that induce a keratinocyte phenotype expressed in psoriatic lesions.
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UM4D4 (CDw60) T 细胞被划分到银屑病皮肤中并释放诱导银屑病皮损中表达的角质形成细胞表型的淋巴因子。
DOI：
10.1111/1523-1747.ep12484908
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Chan,LS
中科院分区：
文献类型：
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作者：
Baadsgaard,O;Tong,P;Elder,JT;Hansen,ER;Ho,V;Hammerberg,C;Lange-Vejlsgaard,G;Fox,DA;Fisher,G;Chan,LS
UM4D4 （CDw60）是一种新的抗原非依赖性T细胞激活途径的表面分子，被发现在病变性银屑病T细胞上高表达。为了检查UM4D4是否代表银屑病T细胞的T细胞激活途径，从急性皮肤病变中启动T细胞系，并通过限制稀释克隆。通过t细胞受体基因重排分析证实了克隆性。所有t细胞克隆，无论是CD4+2H4+CD8-、CD4+2H4-CD8-、CD4-CD8+CD11b-，均表达UM4D4，并被抗UM4D4单克隆抗体激活。皮损性银屑病t细胞克隆在抗um4d4诱导的增殖程度以及IL-2和γ -干扰素的产生方面存在异质性。抗um4d4激活释放的淋巴因子能够诱导培养的正常角质形成细胞表达ICAM-1和HLA-DR。因此，银屑病皮肤t细胞上UM4D4的高表达提供了一种可能在银屑病病变环境中起作用的t细胞活化的替代机制。事实上，通过UM4D4分子激活病变t细胞导致淋巴因子的释放，直接诱导角质形成细胞表达银屑病皮损中显示的表型。
UM4D4 (CDw60), the surface molecule of a novel antigen- independent T-cell activation pathway, was found to be highly expressed on lesional psoriatic T cells. To examine whether UM4D4 represents a T-cell activation pathway for psoriatic T cells, a T-cell line was initiated from an acute skin lesion and cloned by limiting dilution. Clonality was verified by analysis of T-cell receptor gene rearrangement. All T-cell clones tested, whether CD4+2H4+CD8-,CD4+2H4-CD8-, or CD4-CD8+CD11b-, expressed UM4D4 and were activated by the monoclonal antibody anti-UM4D4. Lesional psoriatic T-cell clones were heterogeneous in the degree of anti-UM4D4-induced proliferation and in their production of IL-2 and gamma-interferon. Lymphokines released by anti-UM4D4 activation were capable of inducing ICAM-1 and HLA-DR expression on cultured normal keratinocytes. Thus, the high expression of UM4D4 on T-cells in psoriatic skin provides an alternative mechanism for T-cell activation that may be operative in the psoriatic lesional milieu. Indeed, activation of lesional T-cells through the UM4D4 molecule resulted in release of lymphokines that directly induced keratinocytes to express a phenotype displayed in psoriatic skin lesions.