 Autoimmune diseases occur when the immune system turns against the body's own tissues. Immune cells known as B cells play a primary role in these diseases, producing antibodies that target self-tissues instead of just foreign invaders. All healthy individuals have a small proportion of so-called self-reactive B cells in their immune system, but these cells are typically harmless. The specific event or events provoking the development of autoimmune diseases and only a subset of people therefore remain unclear. But a recent study has proposed that chronic bacterial infection may play an indirect role. Understanding the events triggering these serious diseases could be useful for prevention or treatment. Studies have suggested that stimulation of the immune system by infection might help trigger immune cells to attack the body's own tissues, perhaps because certain pathogens can mimic proteins normally found in the body, or self-antigens. As a result, in reacting to infection, B cells could inadvertently produce antibodies against self-antigens. But this mechanism does not seem to be applicable in autoimmune diseases such as lupus and rheumatoid arthritis. The recent study instead proposes that chronic bacterial infection induces autoimmunity in a more indirect way, causing B cells to undergo changes that then allow the cells to produce a new type of self-reactive antibody. In this work, mice were infected with the bacteria that cause Lyme disease to stimulate the immune response. This bacterial infection specifically stimulated self-reactive B cells in the mice to express a new mutated type of self-reactive antibody. Surprisingly, however, the B cells did not release significant amounts of the antibody, perhaps because of a safety mechanism that counteracts autoimmunity. They were also not mature enough to produce antibodies with a high affinity for self-antigens, which is required for autoimmunity to develop. These results explain why the production of self-reactive antibodies in response to bacteria and other pathogens is uncommon in healthy individuals despite the frequency of chronic human infection. Chronic infection alone, thus, cannot induce autoimmunity. Future research should investigate factors besides infection that may help induce autoimmunity, such as other immune cells, as well as genetic mutations that are associated with autoimmune diseases.