Key result
Spontaneous in vitro anti-nRNP antibody synthesis by lymphocytes from anti-nRNP positive SLE patients was significantly higher than controls and was dependent on T4 helper cells.
Observational (n=74)
No
In patients with SLE, elevated anti-nRNP antibody synthesis is driven by hyperactive nRNP-reactive T4 cells, highlighting a specific immunoregulatory defect.
T4-dependent anti-nRNP synthesis may mark SLE immunoregulatory defects; leaves open whether targeting these cells alters disease course.
The cellular mechanism of anti-nRNP antibody synthesis in patients with systemic lupus erythematosus (SLE) was studied by nRNP-specific solid-phase radioimmunoassay.Spontaneous in vitro anti-nRNP antibody synthesis by lymphocytes from immunodiffusion determined anti-nRNP antibody positive, anti-Sm antibody negative (anti-nRNP positive) SLE patients were significantly higher than by those from the controls. In addition, similar amounts of anti-nRNP antibody were synthesized spontaneously in both active and inactive stage. The reconstitution experiments revealed that B cells and T cells from anti-nRNP positive SLE must cooperate to synthesize anti-nRNP antibody whether with nRNP stimulation or not. Accordingly, B cells and T cells may be activated in vivo due to unknown causes, and anti-nRNP antibody synthesis in response to nRNP was T-cell dependent.T8 cells from anti-nRNP positive SLE patients could suppress anti-nRNP antibody synthesis by autologous B cells, and in correlation with amounts of anti-nRNP antibody synthesized by their whole lymphocytes, their T4 cells could enhance anti-nRNP antibody synthesis by autologous B cells in response to nRNP. These results indicate that elevated anti-nRNP antibody synthesis in response to nRNP in patient with anti-nRNP positive SLE is due to the abnormality of T4 cells, and hyperactivity of nRNP reactive T4 cells may, in part, be responsible for deficient regulation of anti-nRNP antibody synthesis. These findings may lend further insight into understanding of various immunoregulatory defects in SLE.
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Osamu Hosono (1987) conducted an observational in Systemic lupus erythematosus (n=74). Lymphocytes from anti-nRNP positive SLE patients vs. Lymphocytes from healthy controls and anti-nRNP negative SLE patients was evaluated on Spontaneous in vitro anti-nRNP antibody synthesis (cpm). Spontaneous in vitro anti-nRNP antibody synthesis by lymphocytes from anti-nRNP positive SLE patients was significantly higher than controls and was dependent on T4 helper cells.
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