Elkon K B, Bonfa E, Llovet R, Eisenberg R A
Division of Rheumatic Diseases, Cornell University Medical Center, New York 10021.
J Immunol. 1989 Sep 1;143(5):1549-54.
Anti-Sm and anti-ribosomal P protein antibodies show a high degree of specificity for the disease SLE. To determine whether a relationship between these two autoantibodies existed, the frequency of anti-P was determined in sera with and without anti-Sm activity. Of sera from lupus patients with anti-Sm 18/65 (28%), and 6/55 (11%) of sera without anti-Sm had anti-P as determined by an ELISA using a recombinant P2-beta-galactosidase fusion protein as Ag (p less than 0.05). The levels of anti-P were significantly higher in sera containing anti-Sm (0.37 +/- 0.45) than in sera without anti-Sm antibodies (0.18 +/- 0.20) (p less than 0.01). Similarly, a significantly higher proportion of anti-P positivity was found in autoimmune MRL/Mp-lpr/lpr mice positive for anti-Sm (11/53 = 21%) compared to age- and sex-matched mice without anti-Sm (3/53 = 6%) (p less than 0.05). The IgG subclass distributions for anti-Sm and anti-P antibodies were similar in the MRL mice (IgG2a greater than IgG2b greater than IgG3 greater than IgG1). The association did not reflect polyclonal B cell activation in a proportion of MRL mice because no significant differences were observed in anti-DNA, antichromatin or total serum IgG levels in mice with and without anti-Sm or, in mice positive for both anti-P and anti-Sm compared to mice positive for anti-Sm alone. Cross-inhibition experiments excluded the possibility that the Sm and P protein Ag shared a common epitope. Longitudinal measurement of anti-P and anti-Sm antibody levels by ELISA in three mice indicated that both antibodies first appeared at about 3 to 4 mo of age and fluctuated two- to threefold over 3 to 8 mo with independent peaks of activity. Recent observations regarding a relationship between anti-Sm and autoantibodies to other ribosomal proteins suggest that the association may be explained by an immune response to epitopes coassociated on the ribosome.
抗Sm抗体和抗核糖体P蛋白抗体对系统性红斑狼疮（SLE）疾病具有高度特异性。为了确定这两种自身抗体之间是否存在关联，我们检测了有和没有抗Sm活性的血清中抗P抗体的频率。通过使用重组P2-β-半乳糖苷酶融合蛋白作为抗原的ELISA法检测，65份来自有抗Sm的狼疮患者血清中有18份（28%）存在抗P抗体，而55份无抗Sm活性的血清中有6份（11%）存在抗P抗体（p<0.05）。含有抗Sm的血清中抗P抗体水平（0.37±0.45）显著高于无抗Sm抗体的血清（0.18±0.20）（p<0.01）。同样，与年龄和性别匹配的无抗Sm小鼠（3/53 = 6%）相比，抗Sm阳性的自身免疫性MRL/Mp-lpr/lpr小鼠中抗P阳性的比例显著更高（11/53 = 21%）（p<0.05）。在MRL小鼠中，抗Sm和抗P抗体的IgG亚类分布相似（IgG2a>IgG2b>IgG3>IgG1）。这种关联并不反映部分MRL小鼠中的多克隆B细胞激活，因为在有和没有抗Sm的小鼠中，以及与仅抗Sm阳性的小鼠相比，抗P和抗Sm均阳性的小鼠中，抗DNA、抗染色质或总血清IgG水平均未观察到显著差异。交叉抑制实验排除了Sm和P蛋白抗原共享共同表位的可能性。通过ELISA对三只小鼠进行抗P和抗Sm抗体水平的纵向测量表明，两种抗体均在约3至4月龄时首次出现，并在3至8个月内波动两到三倍，且有独立的活性峰值。最近关于抗Sm与其他核糖体蛋白自身抗体之间关系的观察表明，这种关联可能是由对核糖体上共关联表位的免疫反应所解释的。
