Tráfico leucocitario y trastorno inflamatorio

  1. Prieto Martín, A.
  2. Barbarroja Escudero, J.
  3. Gómez Lahoza, A.M.
  4. Monserrat Sanz, J.
Revista:
Medicine: Programa de Formación Médica Continuada Acreditado

ISSN: 0304-5412

Any de publicació: 2017

Sèrie: 12

Número: 24

Pàgines: 1408-1417

Tipus: Article

DOI: 10.1016/J.MED.2016.12.010 DIALNET GOOGLE SCHOLAR

Altres publicacions en: Medicine: Programa de Formación Médica Continuada Acreditado

Objectius de Desenvolupament Sostenible

Resum

ResumenIntroducción Las células inmunes patrullan el organismo buscando agentes patógenos que estimularán la producción de mediadores y la extravasación leucocitaria. Inicio de la respuesta inflamatoria (RI) local Las células infectadas y las células centinela inician la RI. El endotelio se activa y se extravasan líquidos, moléculas solubles y leucocitos. Propagación de la RI Líquidos, moléculas y células drenan desde el foco infeccioso propagando la RI a los órganos linfoides secundarios (OLS), donde las células dendríticas presentarán los antígenos (Ag) a los linfocitos T, y los complejos Ag-complemento estimularán a los linfocitos B. Repercusión sistémica de la RI La linfa eferente transportará mediadores inflamatorios hacia la circulación sanguínea desencadenando la respuesta de fase aguda en bazo, hígado y médula ósea. Respuesta adaptativa en los OLS Los linfocitos Ag-específicos iniciarán la respuesta clonal contra el patógeno y se diferenciarán en células efectoras y memoria. Las células efectoras vuelven a la sangre y a los tejidos infectados donde forman agregados de células linfoides (granulomas y folículos linfoides ectópicos) y eliminan al patógeno. Respuesta clínica La producción aumentada de mediadores solubles de la RI da lugar a patologías. Estos mediadores de la extravasación leucocitaria son posibles dianas terapéuticas en el control de la RI.

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Fuente de los datos: Dialnet