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When the Immune System Turns on the Body: Mechanisms of Overreaction

1The Logic of Immune Activation: Why Restraint Is the Default2Breaking Tolerance: How Self-Reactive Responses Escape Control3Effector Mechanisms of Self-Damage: How Immune Attack Injures Tissue4Allergy: Overreaction to a Harmless Target5Cytokine Storm: When Amplification Replaces Control6Connecting the Mechanisms: Shared Principles and Points of Intervention
Breaking Tolerance: How Self-Reactive Responses Escape Control

When Peripheral Tolerance Fails

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Peripheral tolerance rests on regulatory T cells and inhibitory receptors. It can fail in three ways. Regulatory T cells may lose suppressive capacity, letting self-reactive cells expand. Inhibitory signaling may weaken, lowering the threshold so a self-reactive cell now gets enough costimulation. Or bystander activation occurs: during a strong infection, local cytokines supply the missing costimulatory context, and a self-reactive lymphocyte activates without recognizing the pathogen at all.
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Three routes to peripheral tolerance failure

Peripheral tolerance can fail through loss of regulatory T cell suppression, through weakened inhibitory receptor signaling that lowers the activation threshold, or through bystander activation in an inflamed environment. Each route removes a different restraint, but all three allow a self-reactive lymphocyte to receive the signals it needs to respond.

Bystander activation during infection

A lymphocyte specific for a self-antigen sits quietly in a tissue. A nearby infection drives intense local cytokine release. Those cytokines provide the costimulatory context the self-reactive cell lacked, and it activates without ever recognizing the pathogen. The infection triggered the response, but the response is not aimed at the pathogen.

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