Inflammatory bowel diseases: An immunological approach Enfermedad inflamatoria intestinal: Una mirada inmunológica

Sepulveda S.E.; Beltrán C.J.; Peralta, A; Rivas, P; Rojas, N; Hermoso M.A.; Figueroa C.; Quera, R

Keywords: recruitment, polymorphism, transcription, protein, diagnosis, disease, humans, diseases, human, genetics, receptor, domain, enteritis, review, colitis, factor, bowel, immunology, predisposition, caspase, genetic, ulcerative, signaling, toll, interleukins, adaptor, differential, tlr4, 4, 3, inflammatory, interleukin, derivative, toll-like, Polymorphism,, protein,, Colitis,, Diagnosis,, to, like, 15, Crohn, GATA, NOD2, GATA3


Inflammatory bowel diseases (IBD) are inflammatory diseases with a multifactorial component that involve the intestinal tract. The two relevant IBD syndromes are Crohn's disease (CD) and ulcerative colitis (UC). One factor involved in IBD development is a genetic predisposition, associated to NOD2/CARD15 and Toll-like receptor 4 (TLR4) polymorphisms that might favor infectious enterocolitis that is possibly associated to the development of IBD. The identification of specific immunologic alterations in IBD and their relationship to the etiology of the disease is a relevant research topic. The role of intra and extracellular molecules, such as transcription factors and cytokines that are involved in the inflammatory response, needs to be understood. The relevance of immunologic molecules that might drive the immune response to a T helper (Th) 1, Th 2 or the recently described Th 17 phenotype, has been demonstrated in animal models and clinical studies with IBD patients. CD and UC predominantly behave with a Th 1 and Th 2 immune phenotype, respectively. Recently, an association between CD and Th 17 has been reported. The knowledge acquired from immunologic and molecular research will help to develop accurate diagnostic methods and efficient therapies.

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Título de la Revista: REVISTA MEDICA DE CHILE
Volumen: 136
Número: 3
Editorial: Sociedad Médica de Santiago
Fecha de publicación: 2008
Página de inicio: 367
Página final: 375