Inflamación, activación del endotelio vascular y trombosis

  1. Prieto Martín, A. 1
  2. A. Pérez Gómez 2
  3. A.M. Gómez Lahoz 1
  4. J. Barbarroja Escudero 2
  1. 1 Departamento de Medicina y Especialidades Médicas. Universidad de Alcalá. Alcalá de Henares. Madrid. España
  2. 2 Departamento de Medicina y Especialidades Médicas. Universidad de Alcalá. Alcalá de Henares. Madrid. España Servicio de Enfermedades del Sistema Inmune. Hospital Universitario Príncipe de Asturias. Alcalá de Henares. Madrid. España
Journal:
Medicine: Programa de Formación Médica Continuada Acreditado

ISSN: 0304-5412

Year of publication: 2021

Issue Title: Enfermedes del sistema inmune (VI)

Series: 13

Issue: 33

Pages: 1906-1916

Type: Article

DOI: 10.1016/J.MED.2021.05.004 DIALNET GOOGLE SCHOLAR

More publications in: Medicine: Programa de Formación Médica Continuada Acreditado

Abstract

Inflammation is a defense response that detects, contains, and eradicates threats. Defects in the regulation of its magnitude and duration contribute to the development of pathologies. Sentinel and vascular endothelial cells are activated, produce mediators, and favor the extravasation of leukocytes, defense molecules, and fluids which, after moving through the inflamed tissue, are transported through the lymph. Mediators and antigens arrive at the secondary lymph nodes, where they generate clones of cells that specifically recognize the pathogen. Mediators, antibodies, and lymphocytes specific to the pathogen return to the blood, where they will locate the pathogen in the inflamed tissue and attack it. Following elimination of the pathogen, the inflammation resolves and the injured tissue is repaired. Failure to eliminate it impedes resolution of the disease and inflammation can propagate, become chronic, and intensify through the formation of ectopic lymphoid structures in the inflamed tissues. Exacerbation of inflammatory processes can produce endothelial damage and require the activation of immunosuppressive mechanisms such as myeloid-derived suppressor cells. Lastly, there is debate on the participation of inflammatory processes in the formation and resolution of thrombi.

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