Autoantibody to ribosomes and systemic lupus erythematosus

Sera from a patient with systemic lupus erythematosus (SLE), tested by indirect immunofluorescence on frozen tissue sections, gave granular cytoplasmic staining of hepatocytes, gastric chief cells, exocrine cells of the pancreas and submandibular glands, and cerebellar Purkinje cells. In acetone-fixed monolayers of rat embryonic fibroblasts, 3T3 cells, mouse neuroblastoma cells, and cells from a human melanoma and colon carcinoma cell line, the sera stained perinuclear cytoplasmic granules which radiated out towards the cell periphery. More mature and differentiated fibroblasts from rat of human foetal lung showed staining of reticular cytoplasmic structures corresponding to phase-dense rough endoplasmic reticulum (RER). Nucleoli were prominently stained in all cultured cells. Serum absorption with ribosomes inhibited all antibody activity but absorption with RNA or with RNase-treated ribosomes resulted only in partial inhibition. Monolayers of RNase-treated fibroblasts gave weaker staining reactions compared to control untreated cultures. These observations suggest that the autoantibody is directed against ribosomal RNA and ribosomal protein present in cytoplasmic polyribosomes, in RER and in nucleoli.