Role of class-II major histocompatibility complex (MHC)-antigen-positive donor leukocytes in transfusion-induced alloimmunization to donor class-I MHC antigens
Role of class-II major histocompatibility complex (MHC)-antigen-positive donor leukocytes in transfusion-induced alloimmunization to donor class-I MHC antigens
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DOI：
10.1182/blood.v92.2.690.414k12_690_694
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发表时间：
1998-07-15
期刊：
影响因子：
20.3
通讯作者：
del Rosario, MLU
中科院分区：
文献类型：
--
作者：
Kao, KJ;del Rosario, MLU
已有研究表明，外周血单核白细胞（MNL）负责输血诱导的对供体主要组织相容性复合体（MHC）抗原的同种免疫，然而，尚不清楚MNL的哪个亚群负责这种免疫反应。由于消除ii类MHC抗原阳性的乘客白细胞有效地延长了同种异体移植物的存活时间，因此有假设认为ii类阳性的MNL负责使输血受体免疫供体MHC抗原。为了验证这一假设，使用了两种不同的方法。首先，我们比较了ii类阳性细胞耗尽前后BALB/c小鼠外周血MNL的同种抗原性（H-2(d)）。用CBA小鼠（H-2(k)）作为输血受体。采用流式细胞术和酶联免疫分析法检测供体1类H-2抗原的抗体形成情况。在每周输4次耗尽ii类阳性细胞的MNL后，只有25%的受体小鼠产生针对供体H-2(d)抗原的抗体。相比之下，所有输入对照MNL的小鼠都获得了免疫。其次，我们研究了来自C57BL/6小鼠（H-2(b)）的外周MNL在H-2不同受体小鼠中纯合缺乏ii类MHC分子的异体抗原性。输入ii类MHC分子缺陷MNL后，0%的BALB/c、40%的C57BR和25%的cba受体小鼠产生针对供体H-2(b)抗原的抗体。所有对照受体小鼠均免疫。对照组的抗体活性也高于接受免疫的治疗组。因此，我们的研究表明，ii类MHC抗原阳性的MNL在输血诱导的对供体i类MHC抗原的同种免疫中发挥了重要作用。这些结果也支持这样的假设，即由供体ii类阳性MNL直接向输血受者的免疫系统呈递抗原对于启动供体MHC抗原的体液免疫反应至关重要。(C) 1998年由美国血液病学会出版。
It has been shown that peripheral-blood mononuclear leukocytes (MNL) are responsible for transfusion-induced alloimmunization to donor major histocompatability complex (MHC) antigens, However, it is not known which subset of MNL is responsible for this immune response. Because elimination of class-II MHC antigen-positive passenger leukocytes effectively prolongs the survival of allografts, it has been hypothesized that class-II positive MNL are responsible for immunizing transfusion recipients to donor MHC antigens. To test this hypothesis, two different approaches were used. First, we compared the alloantigenicity of BALB/c mice (H-2(d)) peripheral blood MNL before and after depletion of class-II positive cells. CBA mice (H-2(k)) were used as transfusion recipients. Antibody development to donor class-1 H-2 antigens was determined by flow cytometry and enzyme-linked immunoassay. After four weekly transfusions of MNL depleted for class-II positive cells, only 25% of recipient mice developed antibodies to donor H-2(d) antigens. In contrast, all mice transfused with control MNL became immunized. Second, we studied the alloantigenicity of peripheral MNL from C57BL/6 mice (H-2(b)) with homozygous deficiency of class-II MHC molecules in H-2 disparate recipient mice. After transfusions with class-II MHC molecule-deficient MNL, 0% of BALB/c, 40% of C57BR, and 25% of CBA-recipient mice developed antibodies to donor H-2(b) antigen. All control recipient mice were immunized. The antibody activities of the controls were also higher than those in the treatment group who became immunized. Thus, our study shows that class-II MHC antigen-positive MNL play a significant role in transfusion-induced alloimmunization to donor class-I MHC antigens. The results also support the hypothesis that direct antigen presentation by donor class-II positive MNL to the immune system of transfusion recipients is critical for the initiation of humoral immune response to donor MHC antigens. (C) 1998 by The American Society of Hematology.