We have isolated and characterized a novel antibody from a patient with polymyositis, which precipitates threonine tRNA and an unknown small RNA molecule from 32P‐labeled HeLa extract. Fingerprint analysis showed that the human threonine tRNA precipitated was nearly identical to the murine tRNA described by Harada [(1978) Seikagaku 50, 397–411]. Nucleotide analysis suggested that the other small RNA molecule might be transfer RNA. Since phenol extraction resulted in the loss of immunoprecipitability, the protein portion was presumed to be involved in the recognition of the antigen. Immunofluorescence staining of HeLa cells with the antibody clearly demonstrated that the antigen was located predominantly in the cytoplasm.

A patient with systemic lupus erythematosus (SLE) developed amegakaryocytic thrombocytopenic purpura. The absence of a drug relationship or other identifiable underlying cause madeus consider this to be a rare manifestation of SLE. Her thrombocytopenia, which initially appeared to be steroid-resistant, ultimately improved following a prolonged high-dose prednisolone therapy. To our knowledge, this is the second case of amegakaryocytic thrombocytopenia associated with SLEin the literature. The possibility that amegakaryocytic thrombocytopenia in SLE can be caused by cellular rather than humoral immunologic mechanism was discussed.

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The in vitro Fc receptor function of monocytes as measured by using soluble immunecomplexes (IC) consisting of ovalbumin and 12SI-labeled antibody to ovalbumin was examined in serum-free medium. Adherent monocytes were obtained from peripheral blood of 18 patients with systemic lupus erythematosus (SLE; 6 active, 12 inactive) and 13 normal controls. 5xlO5 monocytes were incubated with soluble IC containing 20 ng IgG for 16 hr at 4°C, and for 4 hr and 16 hr at 37°C, and then cell-associated and acid-soluble radioactivities were counted. After 16-hr incubation at 4°C, there was no significant difference in the amount of cell-associated IC between monocytes from SLEpatients and those from normal controls. After 4 hr incubation at 37°C, monocytes from patients with active SLE bound and phagocytized more IC than those from patients with inactive SLE or from normal controls (P<0.01). After 16 hr incubation at 37°C, degradation of soluble IC by monocytes from patients with active SLE greatly increased (P<0.003).These findings were discussed in relation to the possible pathophysiologic role of the mononuclear phagocyte system in SLE.

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