A unique phenotype of skin-associated lymphocytes in humans. Preferential expression of the HECA-452 epitope by benign and malignant T cells at cutaneous sites.
A unique phenotype of skin-associated lymphocytes in humans. Preferential expression of the HECA-452 epitope by benign and malignant T cells at cutaneous sites.
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发表时间：
1990
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通讯作者：
L. Picker;S. Michie;L. Rott;E. Butcher
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作者：
L. Picker;S. Michie;L. Rott;E. Butcher
有人提出，皮肤是免疫系统的功能独特的隔室，尽管支持这一假设的直接证据很少。在这里，我们表明，在皮肤部位的淋巴细胞群体可以区分从其他类似的人群在非皮肤部位的单克隆抗体HECA-452定义的表位的优先表达。该MAb识别存在于约16%外周血T细胞上的主要为200-kd的细胞表面糖蛋白，包括CD 4+和CD 8 + T细胞（分别为17%和11%HECA-452+）以及携带TCR-δ的T细胞（32%+）。大多数胸腺细胞（99%）缺乏HECA-452抗原表达，并且基本上所有HECA-452+外周血T细胞都存在于粘附分子高、CD 45 R低的推定记忆细胞亚群中，结果表明HECA-452表达是抗原刺激的结果。然而，HECA-452抗原不是常规的活化抗原，因为它不被外周血T细胞的有丝分裂原刺激上调。最重要的是，在54个不同的正常/反应性淋巴组织和慢性炎症部位的标本中，淋巴细胞HECA-452表达和皮肤位置有明显的相关性。在皮外部位（n = 38），这些组织的T细胞区域内仅约5%的淋巴细胞表达该抗原，而在炎性皮肤病变（n = 16）中，85%为HECA-452+。在一系列T细胞淋巴瘤中也发现了HECA-452表达与皮肤位置的相关性。18例表皮型蕈样肉芽肿（斑片/斑块）中16例恶性细胞为HECA-452+，7例非蕈样肉芽肿性外周T细胞淋巴瘤中2例为HECA-452+。相反，这种抗原在胸腺（成淋巴细胞）淋巴瘤（n = 14），非表皮（肿瘤）期蕈样肉芽肿（n = 5），和非皮肤外周T细胞淋巴瘤（n = 15）中不表达。在淋巴细胞中，皮肤T细胞优先表达HECA-452决定簇支持皮肤构成免疫学上独特的淋巴组织的假设，并表明该分子可能在淋巴细胞归巢至皮肤或淋巴细胞与表皮的相互作用中发挥作用。
It has been proposed that the skin is a functionally unique compartment of the immune system, although little direct evidence supporting this hypothesis has been presented. Here we show that lymphocyte populations at cutaneous sites can be differentiated from otherwise similar populations at noncutaneous sites by their preferential expression of an epitope defined by the MAb HECA-452. This MAb recognizes a predominantly 200-kd cell-surface glycoprotein present on about 16% of peripheral blood T cells, including both CD4+ and CD8+ T cells (17% and 11% HECA-452+, respectively), as well as TCR-delta-bearing T cells (32%+). Most thymocytes (99%) lacked HECA-452 antigen expression, and essentially all the HECA-452+ peripheral blood T cells were found in the adhesion molecule high, CD45R low putative memory cell subset, findings suggesting that HECA-452 expression develops peripherally as a consequence of antigenic stimulation. However, the HECA-452 antigen is not a conventional activation antigen because it was not upregulated with mitogen stimulation of peripheral blood T cells. Most significantly, among 54 diverse specimens of normal/reactive lymphoid tissues and sites of chronic inflammation, there was a clear association of lymphocyte HECA-452 expression and cutaneous location. In extracutaneous sites (n = 38) only about 5% of lymphocytes within the T-cell areas of these tissues expressed this antigen, whereas in inflammatory skin lesions (n = 16), 85% were HECA-452+. The association of HECA-452 expression and cutaneous location was also seen in a series of T-cell lymphomas. The malignant cells of 16 of 18 cases of epidermotropic (patch/plaque) stage mycosis fungoides were HECA-452+, as well as 2 of 7 nonmycosis fungoides peripheral T-cell lymphomas in skin. In contrast, this antigen was not expressed in thymic (lymphoblastic) lymphomas (n = 14), nonepidermotropic (tumor) stage mycosis fungoides (n = 5), and noncutaneous peripheral T-cell lymphomas (n = 15). Among lymphocytes, the preferential expression of the HECA-452 determinant by cutaneous T cells supports the hypothesis that the skin constitutes a immunologically unique lymphoid tissue and suggests that this molecule may play a role in either lymphocyte homing to skin or in lymphocyte interactions with the epidermis.