Gamberale Romina, Geffner Jorge R, Giordano Mirta
Laboratorio de Immunologia, Instituto de Investigaciones Hematológicas, Academia de Medicina, Buenos Aires, Argentina.
Leuk Lymphoma. 2002 Feb;43(2):251-5. doi: 10.1080/10428190290006008.
The progressive accumulation of B-cell chronic lymphocytic leukemia (B-CLL) cells in vivo is attributed to resistance to apoptosis, although this can be modulated in vitro by a variety of cellular and humoral factors (cell-cell, cell-matrix interactions, cytokines). We have previously reported that IgG immune complexes (IC) delay B-CLL cell apoptosis through a paracrine mechanism, which depends on monocytes and NK cells. On the other hand, despite the fact that IC effectively bind to type II Fc gammaRs expressed on B-CLL cells, they are unable to deliver transmembrane signals. We speculate that this lack of responsiveness of resting B-CLL cells to IC could be overcome by activation. The analysis of this possibility would be relevant since the presence of circulating IC is a common feature in B-CLL patients.
B细胞慢性淋巴细胞白血病（B-CLL）细胞在体内的渐进性积累归因于对细胞凋亡的抗性，尽管在体外这种抗性可被多种细胞和体液因子（细胞-细胞、细胞-基质相互作用、细胞因子）调节。我们之前报道过，IgG免疫复合物（IC）通过一种旁分泌机制延迟B-CLL细胞凋亡，该机制依赖于单核细胞和自然杀伤细胞。另一方面，尽管IC能有效结合B-CLL细胞上表达的II型FcγR，但它们无法传递跨膜信号。我们推测，静止的B-CLL细胞对IC缺乏反应性可通过激活来克服。由于循环IC的存在是B-CLL患者的一个常见特征，因此分析这种可能性将具有重要意义。
