Hypothetical representation. The image shows the hypothetical representation of the mechanisms involved (A) in sensitizing infected patients to PF4 and (B) favoring further development of HIT when treated by heparin (adapted from Krauel et al's Figure 6). (A) Bacteria can induce the release of PF4, which then binds polyanions present on the bacterial surface. This interaction triggers the synthesis of antibodies specific to modified PF4, which can bind to variable bacterial strains and favor their phagocytosis by granulocytes. (B) After initiation of heparin treatment (particularly in surgical patients), PF4/heparin complexes are formed, mimic PF4 bound to bacteria and thus trigger the synthesis of modified PF4-specific antibodies in sensitized patients. Anti-PF4/polyanion IgG antibodies strongly activate platelets in some cases and promote the development of HIT.