Bocchieri M H
Department of Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107.
Immunology. 1989 Apr;66(4):526-31.
T-cell clones were derived from autoimmune prone (NZB) and non-autoimmune (C58) strains of mice and tested for their effects in several assays of B-cell responsiveness. Clones from the C58 strain suppressed lipopolysaccharide LPS-stimulated B-cell proliferation, activation and immunoglobulin synthesis. In contrast, an NZB-derived clone enhanced these measures of B-cell response. The effects of the NZB clone were more notable on splenic target populations taken from mice 6 months of age or older. MHC-compatible DBA/2 spleen cells also showed enhancement of B-cell activation, but not of immunoglobulin synthesis by the NZB clone. It has been shown previously that all of the clones suppress T-cell proliferative responses. A potentially important skewing of the immune system toward humoral rather than cellular responses is therefore mediated by this clone derived from an autoimmune strain.
T细胞克隆源自自身免疫易感(NZB)和非自身免疫(C58)品系的小鼠,并在几种B细胞反应性检测中测试其作用。来自C58品系的克隆抑制脂多糖(LPS)刺激的B细胞增殖、活化和免疫球蛋白合成。相比之下,一个源自NZB的克隆增强了这些B细胞反应指标。NZB克隆对取自6个月及以上小鼠的脾脏靶细胞群体的作用更显著。MHC相容的DBA/2脾细胞也显示出B细胞活化增强,但NZB克隆未增强其免疫球蛋白合成。先前已表明,所有克隆均抑制T细胞增殖反应。因此,源自自身免疫品系的该克隆介导了免疫系统向体液而非细胞反应的潜在重要偏向。