Mecanismos de daño en las reacciones de hipersensibilidad

  1. Díaz Martín, D. 1
  2. Muñoz, L. 2
  3. Álvarez-Mon Soto, M. 3
  1. 1 Laboratorio de Enfermedades del Sistema Inmune y Oncología. Departamento de Medicina y Especialidades Médicas. Universidad de Alcalá. Alcalá de Henares. Madrid. España
  2. 2 Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd). Instituto de Salud Carlos III. Madrid. España
  3. 3 Laboratorio de Enfermedades del Sistema Inmune y Oncología. Departamento de Medicina y Especialidades Médicas. Universidad de Alcalá. Alcalá de Henares. Madrid. España Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd). Instituto de Salud Carlos III. Madrid. España Servicio de Medicina Interna. Reumatología y Autoinmunidad. 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: 1867-1881

Type: Article

DOI: 10.1016/J.MED.2021.05.001 DIALNET GOOGLE SCHOLAR

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

Sustainable development goals

Abstract

The immune system is necessary to defend the host against infections. However, immune responses themselves are able to cause injury and disease in tissues. Damaging or pathological immune reactions are called hypersensitivity reactions. An immune response to an antigen can produce sensitivity to a challenge from this antigen and thus, hypersensitivity is a reflection of excessive or aberrant immune responses. Historically, hypersensitivity reactions due to immune responses were classified by Gell and Coombs into four types. Type I hypersensitivity reactions were immediate allergic reactions mediated by IgE antibodies, with activation of mast cells being the main final effector mechanism. Type II and III hypersensitivity responses were defined as those driven by IgG antibodies specific to the antigen, with the final effector mechanism being the complement (type II) or FcR bearing cell effectors (type III). Lastly, they described type IV hypersensitivity responses, which are driven by cell effectors, including lymphocytes and a variety of myeloid cell types. Disorders caused by inappropriate immune responses are called hypersensitivity diseases. This term arises from the clinical definition of immunity as sensitivity, which is based on the observation that a subject who has been exposed to an antigen exhibits a detectable reaction or is sensitive to later encounters with that antigen.

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