Martin T, Pasquali J L
Laboratoire d'Immunopathologie, Hôpital Civil CHU, Strasbourg, France.
Leuk Lymphoma. 1992 May;7(1-2):55-62. doi: 10.3109/10428199209053602.
IgM-RF B cell precursors are abnormally overrepresented in "well differentiated" lymphoid monoclonal proliferations while data on less mature lymphoid malignancies are still awaited. This nevertheless suggests that RF activity plays a role in the transforming process perhaps by inducing constant stimulation of the precursor B cells. Despite the preferential use of similar VH and VL genes with little or no somatic hypermutations in both malignant B-cell CLL and nonmalignant mixed cryoglobulinemia, these proliferations do differ in CD5 membrane expression and in their clinical evolution. One possibility could be that CD5 glycoprotein is lost during maturation of the lymphocyte into a secreting cell as suggested by data on Waldenström's disease and the LES-CLL and by in vitro studies. Alternatively, CD5 expression could play an additional direct role in malignant transformation as suggested by recent data on the CD5 receptor ligand. Further data on the proliferating cells in both situations as well as on the genetic control of CD5 expression in B cells and its physiology should shed additional light on the mechanisms of B-cell malignancy.
IgM类风湿因子（RF）B细胞前体在“高分化”淋巴样单克隆增殖中异常过度表达，而关于不太成熟的淋巴样恶性肿瘤的数据仍有待获取。然而，这表明RF活性可能通过诱导前体B细胞的持续刺激在转化过程中发挥作用。尽管在恶性B细胞慢性淋巴细胞白血病（CLL）和非恶性混合性冷球蛋白血症中都优先使用相似的重链可变区（VH）和轻链可变区（VL）基因，且几乎没有或没有体细胞超突变，但这些增殖在CD5膜表达及其临床演变方面确实存在差异。一种可能性是，正如华氏巨球蛋白血症、LESS-CLL的数据以及体外研究表明的那样，CD5糖蛋白在淋巴细胞成熟为分泌细胞的过程中丢失。或者，正如最近关于CD5受体配体的数据所表明的，CD5表达可能在恶性转化中发挥额外的直接作用。关于这两种情况下增殖细胞的更多数据，以及B细胞中CD5表达的遗传控制及其生理学，应该会进一步阐明B细胞恶性肿瘤的机制。
