Kadin M E, Muramoto L, Said J
Department of Pathology, Beth Israel Hospital, Boston, MA 02215.
Am J Pathol. 1988 Feb;130(2):345-53.
Expression of T-cell antigens by Reed-Sternberg (RS) cells has not been detected in most studies of Hodgkin's disease (HD). The authors employed an improved method of fixation (paraformaldehyde-lysine-periodate), which sharply defined cell borders and revealed T-cell antigens on RS cells in 8 of 30 (27%) cases of HD. Antigen-specific staining was confirmed by immunoelectron microscopy. RS cells expressed T11 (8/8 cases), Leu-3 or T4 (4/8 cases), Leu-4 or T3 (3/8 cases), but not other T-cell specific antigens (Leu-1, T8, T6, 3A1). RS cells were negative for leukocyte common antigen (LCA/T200), in contrast to positive LCA/T200 staining of RS-like cells in T-cell lymphomas. RS cells in all HD cases were positive for Ki-1 and/or Leu-M1 antigens. The percentage of RS cells expressing T-cell antigens was less than 20% (2 cases), 20-50% (3 cases), or greater than 50% (3 cases). This percentage and the specific T-cell antigens expressed varied in tissues from different sites in each of 2 cases. Expression of T-cell antigens by RS cells was found in nodular sclerosis (6 of 20 cases) and mixed cellularity (2 of 5 cases) but not in lymphocyte predominance (2 cases), lymphocyte depletion (1 case), or unclassified types (2 cases). Two cases of nodular sclerosis contained areas of necrosis surrounded by sheets of lacunar cells (syncytial variant of NSHD). Two other cases were associated with cutaneous lymphoma. One of these cases was mixed cellularity HD, which appeared to be confined to the skin. In a second case, tumor cells of similar phenotype (T4+, Ki-1+) were found in skin and lymph nodes of a patient with coexistent mycosis fungoides and HD. These results are consistent with an origin of RS cells from T cells in some cases of nodular sclerosing and mixed cellularity HD. They also suggest that the same cell type, an activated helper T-cell, is involved in the pathogenesis of both skin lesions and lymphadenopathy of some patients with coexistent mycosis fungoides and HD.
在大多数霍奇金病(HD)研究中,未检测到里德-施特恩伯格(RS)细胞表达T细胞抗原。作者采用了一种改进的固定方法(多聚甲醛-赖氨酸-高碘酸盐),该方法能清晰界定细胞边界,并在30例HD病例中的8例(27%)RS细胞上显示出T细胞抗原。免疫电子显微镜证实了抗原特异性染色。RS细胞表达T11(8/8例)、Leu-3或T4(4/8例)、Leu-4或T3(3/8例),但不表达其他T细胞特异性抗原(Leu-1、T8、T6、3A1)。与T细胞淋巴瘤中RS样细胞LCA/T200染色阳性相反,RS细胞白细胞共同抗原(LCA/T200)呈阴性。所有HD病例中的RS细胞Ki-1和/或Leu-M1抗原均为阳性。表达T细胞抗原的RS细胞百分比小于20%(2例)、20 - 50%(3例)或大于50%(3例)。在2例患者中,该百分比以及所表达的特定T细胞抗原在不同部位的组织中有所不同。在结节硬化型(20例中的6例)和混合细胞型(5例中的2例)HD中发现RS细胞表达T细胞抗原,但在淋巴细胞为主型(2例)、淋巴细胞消减型(1例)或未分类类型(2例)中未发现。2例结节硬化型病例含有坏死区域,周围有大片陷窝细胞(结节硬化型HD的合体细胞变体)。另外2例与皮肤淋巴瘤相关。其中1例为混合细胞型HD,似乎局限于皮肤。在第2例中,在一名蕈样肉芽肿与HD并存患者的皮肤和淋巴结中发现了具有相似表型(T4 +、Ki-1 +)的肿瘤细胞。这些结果与某些结节硬化型和混合细胞型HD病例中RS细胞起源于T细胞一致。它们还表明,同一细胞类型,即活化的辅助性T细胞,参与了一些蕈样肉芽肿与HD并存患者皮肤病变和淋巴结病的发病机制。