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Updated: Aug 20, 2026

Pseudofracture: An Acute Peripheral Tissue Trauma Model
Published on: April 18, 2011
Immune complex-mediated tissue injury: a multistep paradigm
Sonia Jancar1, Mariano Sánchez Crespo
1Instituto de Ciências Biomédicas, Universidade de São Paulo, Av. Professor Lineu Prestes 2415, 05508-900 São Paulo, SP, Brazil.
Abstract:
Antigen-antibody complexes can damage tissues by triggering inflammation. Recent studies have enabled the description of a sequence of steps, which depend on the intra- or perivascular location of complex formation. Acute lethal toxicity and circulatory shock as a result of the acute release of inflammatory mediators can occur after intravascular complex formation. The lesions associated with perivascular complexes are characterized by plasma leakage and the recruitment of polymorphonuclear leukocytes. These lesions are modulated by mediators released from endothelial cells, namely nitric oxide, endothelins and lipid mediators, and provide an appropriate basis for the activation of both arms of hemostasis: coagulation and fibrinolysis. The balance between both activation systems can explain the late occurrence of both tissue fibrosis and organ remodeling.
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