Surface antigen specificity of cold-reactive IgM antilymphocyte antibodies in systemic lupus erythematosus.

Surface antigen specificity of cold-reactive IgM antilymphocyte antibodies in systemic lupus erythematosus.
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系统性红斑狼疮冷反应 IgM 抗淋巴细胞抗体的表面抗原特异性。

DOI:
10.1002/art.1780280108
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发表时间:
1985
影响因子:
--
通讯作者:
Winfield,JB
Winfield,JB
中科院分区:
--
文献类型:
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作者:
Yamada,A;Shaw,M;Winfield,JB

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针对B细胞和各种类型的静息和活化T细胞上的已知表面抗原的单克隆抗体被用于几种方法中,以检查IgM抗淋巴细胞抗体在系统性红斑狼疮(SLE)中的特异性。寻找的表面决定簇包括:T3、T11、Leu-1、Leu-8(泛T); T4、T8(T亚群); β2微球蛋白(β 2 m); L243、Leu-10(分别为DR和DS/DC框架);抗Tac(白细胞介素-2受体); 5E 9(转铁蛋白受体);和4F 2、AA 1(其他活化抗原)。第一种策略是基于直接在4°C下或在37°C下调节IgM抗淋巴细胞抗体反应性靶细胞抗原后,SLE血清抑制小鼠单克隆抗体包被的靶细胞和抗小鼠IgG包被的红细胞之间的玫瑰花结形成。显著的玫瑰花结抑制,定义为与10份对照血清的平均值相差> 2个标准差,仅观察到β 2 m(20份SLE血清中有13份为阳性;抑制= 15-58%)。接下来,在4°C下将细胞与SLE血清预孵育后或在调节SLE抗体反应性抗原后,通过流式显微荧光测定法评估单克隆抗体对淋巴细胞染色的相对荧光强度。调制显着减少或消除SLE抗淋巴细胞抗体IgM染色。除β 2 m外,冷或暖温度预孵育均未改变已知表面抗原的相对荧光强度。这些数据证实了抗β 2 m是SLE中常见的特异性抗体,并表明该疾病中的抗淋巴细胞抗体不针对Ia或某些其他功能性目的淋巴细胞抗原。
Monoclonal antibodies to known surface antigens on B cells and on resting and activated T cells of various types were used in several approaches to examine the specificity of IgM antilymphocyte antibodies in systemic lupus erythematosus (SLE). Surface determinants that were sought included: T3, T11, Leu‐1, Leu‐8 (pan‐T); T4, T8 (T subset); β2‐microglobulin (β2m); L243, Leu‐10 (DR and DS/DC framework, respectively); anti‐Tac (interleukin‐2 receptor); 5E9 (transferrin receptor); and 4F2, AA1 (other activation antigens). The first strategy was based on inhibition of rosette formation between mouse monoclonal antibody‐coated targets and antimouse IgG‐coated erythrocytes by SLE sera, either directly at 4°C or after modulation of IgM antilymphocyte antibody‐reactive target cell antigen at 37°C. Significant rosette inhibition, defined as > 2 standard deviations from the mean value for 10 control sera, was seen only for β2m (13 of 20 SLE sera were positive; inhibition = 15–58%). Next, relative fluorescence intensity of lymphocyte staining by monoclonal antibodies was assessed by flow microfluorometry after preincubation of cells with SLE serum at 4°C or after modulation of SLE antibody‐reactive antigen. Modulation markedly reduced or eliminated SLE antilymphocyte antibody IgM staining. Except for β2m, neither cold nor warm temperature preincubations altered the relative fluorescence intensity for the known surface antigens. These data confirm anti‐β2m as a common antibody specificity in SLE and suggest that antilymphocyte antibodies in this disorder are not directed to Ia or to certain other defined lymphocyte antigens of functional interest.