Ayanlar-Batuman O, Shevitz J, Traub U C, Murphy S, Sajewski D
Blood. 1987 Aug;70(2):494-500.
Immunoregulatory T and B cell functions in 15 patients with primary myelodysplastic syndrome (MDS) were studied by measuring the proliferative and the stimulatory capacity of T and B cells, respectively, in autologous (auto) and allogeneic (allo) mixed lymphocyte reaction (MLR). T cell proliferation in the auto MLR was 25% of the control (P less than .02), whereas proliferation in the allo MLR was normal. When control T cells were stimulated by MDS B cells, their proliferative response was only 57% of the control (P less than .01). The mechanism responsible for these abnormalities was studied by determining the capacity of MDS and normal T cells to produce interleukin 2 (IL 2) and to generate IL 2 receptors (IL 2R) following stimulation with control and MDS B cells. In the auto MLR of MDS patients, only 3% +/- 2% of T cells developed IL 2R positivity, whereas in control cultures 12% +/- 2% of T cells were positive, as determined by immunofluorescence, using a monoclonal antibody (MoAb) directed against the IL 2R, and FACS analysis. When MDS T cells were stimulated by control B cells, IL 2R generation and the production of IL 2 were within normal limits. In contrast, when control T cells were stimulated by MDS B cells or control B cells, the MDS B cells induced production of only 26% of IL 2 as compared with control B cells. In parallel experiments, IL 2R generation in control T cells stimulated by either MDS or control B cells was similar. We conclude that in the primary MDS, T and B cell interactions are impaired. Although MDS T cells develop normal quantities of IL 2R and produce normal amounts of IL 2 when stimulated by control B cells, they are markedly impaired when stimulated by self B cells. Similarly, MDS B cells can induce IL 2R generation in control T cells but not in MDS T cells. Myelodysplastic B cells are also defective in inducing IL 2 production by normal T cells in an allo MLR. These in vitro abnormalities strongly suggest that generation of lymphocytes with immunoregulatory functions is impaired in patients with MDS.
通过分别检测15例原发性骨髓增生异常综合征（MDS）患者T细胞和B细胞在自体（auto）和同种异体（allo）混合淋巴细胞反应（MLR）中的增殖能力和刺激能力，研究了其免疫调节性T细胞和B细胞功能。自体MLR中T细胞增殖为对照的25%（P＜0.02），而异体MLR中增殖正常。当对照T细胞被MDS B细胞刺激时，其增殖反应仅为对照的57%（P＜0.01）。通过测定MDS和正常T细胞在被对照和MDS B细胞刺激后产生白细胞介素2（IL - 2）以及生成IL - 2受体（IL - 2R）的能力，研究了这些异常现象的机制。在MDS患者的自体MLR中，通过使用针对IL - 2R的单克隆抗体（MoAb）和流式细胞术分析免疫荧光法测定，仅3%±2%的T细胞出现IL - 2R阳性，而对照培养物中12%±2%的T细胞为阳性。当MDS T细胞被对照B细胞刺激时，IL - 2R生成和IL - 2产生在正常范围内。相反，当对照T细胞被MDS B细胞或对照B细胞刺激时，与对照B细胞相比，MDS B细胞仅诱导产生26%的IL - 2。在平行实验中，被MDS或对照B细胞刺激的对照T细胞中IL - 2R生成相似。我们得出结论，在原发性MDS中，T细胞和B细胞相互作用受损。尽管MDS T细胞在被对照B细胞刺激时产生正常量的IL - 2R并产生正常量的IL - 2，但当被自身B细胞刺激时则明显受损。同样，MDS B细胞可在对照T细胞中诱导IL - 2R生成，但在MDS T细胞中则不能。骨髓增生异常的B细胞在同种异体MLR中诱导正常T细胞产生IL - 2方面也存在缺陷。这些体外异常强烈提示，MDS患者中具有免疫调节功能的淋巴细胞生成受损。
