Patients with systemic lupus erythematosus (SLE) do not get rid of self-attacking B cells even when in symptom-free remission, report Yurasov et al. (page 2255).
Figure 1.
Patients in remission have a lower percentage of autoreactive B cells (black) than do symptomatic SLE patients, but still considerably higher than healthy individuals.
Patients with SLE suffer from chronic inflammation mainly of the connective tissues and organs. Treatment with immunosuppressants or cytotoxic drugs relieves the symptoms of SLE by depleting B cells, but these patients in remission are prone to frequent flare-ups.
During normal B cell development, checkpoints identify and destroy cells that make antibodies against the self. Previous studies revealed high levels of self-reactive antibodies in patients with SLE compared with healthy people, but whether these cells persist in symptom-free remission patients was unknown.
Yurasov et al. used ELISA to look at the reactivity of individual B cell antibodies. They compared individual B cells from patients in remission with those from symptomatic patients as well as healthy individuals. Although patients in remission had fewer self-reactive B cells than symptomatic patients (34.25% versus 44.4%), they still had considerably more than healthy individuals (19.7%). The B cells analyzed by the team were “naive” and thus immature, suggesting that checkpoint failures early in B cell development are the cause of self-reactive antibodies in SLE.
The persistence of self-reactive B cells in remission patients might explain the occasional flare-ups and also suggests that, although the symptoms of SLE might disappear in remission, the faulty checkpoints remain. 