Under normal circumstances, weak interactions between B‑cell

receptors and self‑antigens fail to trigger full activation due to

signalling thresholds that enforce tolerance. In a genetically modified system,

B cells show normal development and receptor diversity but require

significantly less signalling input for activation. Over time, this system

develops circulating autoantibodies and immune complex‑mediated

pathology.

What is the most likely immunological consequence of

lowering this activation threshold?