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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?