Hyperacute Rejection: Antibody-Mediated Vascular Occlusion

Immune Attack Parameters

Preformed antibody titer 50

ABO / HLA mismatch 70%

Complement activity 100%

Simulation speed 1.0×

Graft Status

Perfusion established — monitoring

Lumen occlusion0%

Elapsed time

0.0 min

Antigen sites bound

0 / 40

How it works

Hyperacute rejection is a Type II (antibody-mediated) hypersensitivity reaction. If the recipient already carries antibodies against the donor's ABO blood-group or HLA class I antigens — from a prior transplant, transfusion or pregnancy, or simple blood-type incompatibility — those antibodies bind donor vascular endothelium within minutes of graft reperfusion:

Site binds when:  rand() < k · (titer/100) · (mismatch/100) · dt
Once bound:       occlusion(t+dt) = occlusion(t) + (complement/100) · g · dt
Graft occlusion:  O(t) = mean( occlusion_i )  over all antigen sites i

Bound antibody activates the classical complement cascade (C1q → C3 → C5b-9, the membrane attack complex), which injures the endothelium and exposes tissue factor and von Willebrand factor. That triggers platelet aggregation and fibrin deposition — a thrombus that grows at each bound site (the red particles) and progressively narrows the vessel lumen.

Antibody titer — how much preformed antibody is circulating; higher titer means more binding events per minute.
ABO / HLA mismatch — donor–recipient incompatibility severity; at 0% the crossmatch is negative and almost nothing binds, exactly why every real transplant is screened first.
Complement activity — how fast a bound site converts into an occluding thrombus once antibody has attached.

In practice this reaction is prevented — not treated — by a negative crossmatch and ABO-compatible donor selection before surgery; once thrombosis starts inside the graft it is typically irreversible within minutes to hours.

Circulating antibody Free antigen site Thrombus / occlusion

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