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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

Epitope Spreading: How an Attack Broadens Over Time

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Follow the rounds. The first response targets one self-peptide and damages tissue. That damage releases proteins that were hidden before. Antigen-presenting cells display new peptides from them, and lymphocytes specific for those new epitopes activate. Now the attack has two targets, then three. Each round of damage releases more antigen and recruits more specificities. This is why autoimmune disease often broadens and worsens, and why the original trigger may no longer be needed.
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Epitope spreading is the process by which an autoimmune response expands from an initial target to additional self-antigens. It begins when tissue damage releases proteins that were previously hidden from the immune system. Those proteins are taken up by antigen-presenting cells, processed, and displayed as new peptides. Lymphocytes specific for these newly exposed epitopes are then activated and join the attack.

The consequence is amplification. What started as a response to one self-peptide becomes a response to several, and each new specificity adds more tissue damage, which releases more antigens, which recruits more specificities. The process can become self-sustaining. Epitope spreading explains why autoimmune diseases often worsen over time and why the original trigger may no longer be required once the response has broadened. It also means that the set of targets at diagnosis may differ from the set of targets later in the disease.

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