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Fig. 5 | Arthritis Research & Therapy

Fig. 5

From: Platelets are activated in ANCA-associated vasculitis via thrombin-PARs pathway and can activate the alternative complement pathway

Fig. 5

The proposed cross-talk mechanism among ANCA, neutrophils, complement, and platelets in the pathogenesis of AAV. Neutrophil stimulation with cytokines (such as C5a or TNF-α) and ANCA results in respiratory burst and degranulation, which leads to the release of tissue factor (TF)-bearing microparticles and NETs that subsequently activate the coagulation system and generate thrombin. Thrombin can activate platelets through PARs. Such activated platelets can activate the alternative complement pathway. Additionally, activated neutrophils can also activate the alternative complement pathway via their cell membranes, microparticles, and NETs. This leads to the generation of more C5a, establishing a self-fueling inflammatory amplification loop leading to the vasculitic injury

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