Some pathophysiological contexts favoring the development of autoantibodies
Inducing cause | Pro-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
JA: Conceptualization, Writing—original draft, Writing—review & editing.
JA is consultant for HYPHEN BioMed SAS.
Not applicable.
Not applicable.
Not applicable.
Not applicable.
Not applicable.
© The Author(s) 2024.