Applying the Mechanisms: Which Failure Explains the Scenario? | AI Learning Guide

Use trigger and timing to tell the mechanisms apart. No external trigger and a self-reactive cell that was never removed points to central tolerance failure. Restraint removed, with weakened regulatory or inhibitory control, points to peripheral tolerance failure. A strong local inflammation that supplies costimulation without specific recognition is bystander activation. A response following an infection whose antigen resembles self is molecular mimicry. A target set that broadens over time is epitope spreading. In the post-infection joint scenario, mimicry initiates and spreading amplifies; they work in sequence, not as alternatives.

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Discriminating the mechanisms by trigger and timing

Mechanism

Central tolerance failure
Peripheral tolerance failure
Bystander activation
Molecular mimicry
Epitope spreading

Distinguishing feature

No external trigger; self-reactive cell was never removed
Restraint removed; weakened Treg or inhibitory signaling
Strong local inflammation supplies costimulation without specific recognition
Follows an infection whose antigen resembles self
Target set broadens over time as damage releases new antigens

Post-infection joint inflammation

Joint inflammation appearing weeks after a gastrointestinal infection, with additional joints involved over months, fits molecular mimicry as the initiator and epitope spreading as the amplifier. The post-infection timing identifies mimicry; the progressive broadening identifies spreading. They operate in sequence.