Some pathophysiological contexts favoring the development of autoantibodies

Inducing causePro-thrombotic autoantibody generated

Drug-induced

      Heparin

      Protamine sulfate

      Quinine

      Substitutive therapy

Anti-HPF4, anti-PF4 antibodies

Anti-protamine sulfate antibodies (Plt activation)

Anti-GP1b-IX (Plt activation, thrombocytopenia)

Anti-FVIII, anti-FIX

Infectious diseases

      Varicella

      Adenovirus

      Pharyngeal infection

      Herpes, megalovirus, EBV infections, etc.

Anti-PS, LA

Anti-PT, LA

Anti-PF4

Anti-GP-IIb-IIIa, GPVI, GP1b-IX-V, etc.

Degenerative disease

      Malignancy

      Others

LA

Anti-β2GP1

Anti-PT

Anti-annexin V

Anti-FXIII

Anti-FVIII, anti-vWF, etc.

Others

Various pathological conditions

      Inflammation, NETs

ANCAs

Anti-cytokines

Anti-interferon

Others

Chemicals

      Environmental pollution

      Chemicals

LA, anti-β2GP1

Anti-FXIII

Others

Physiological conditions

      Ageing

      Genetic predisposition

Miscellaneous

ANCAs: anti-neutrophil cytoplasmic antibodies; anti-GP1b-IX: anti-glycoprotein 1b-IX; anti-PT: anti-prothrombin; anti-FVIII: anti-factor VIII; anti-HPF4: anti-heparin-Plt factor 4 (PF4) complexes; EBV: Epstein Barr virus; LA: lupus anticoagulant; NETs: neutrophil extravascular traps; PS: protein S; vWF: von Willebrand factor