RESUMEN
Crohn's disease and ulcerative colitis are idiopathic chronic inflammatory diseases that primarily affect the gastrointestinal tract. The underlying causes remain poorly understood, but there is a growing body of evidence advocating a likely primary pathogenic role for immunodeficiency in the development of Crohn's lesions. Concordantly, a number of congenital immunodeficiencies disrupting the cellular innate immune system strongly predispose to noninfectious, Crohn's-like inflammatory bowel disease. There are case reports and series suggesting that the same may be true for some of the congenital adaptive and complement immunodeficiencies. This review considers and critiques these potential associations.
Asunto(s)
Inmunidad Adaptativa , Colitis Ulcerosa/inmunología , Proteínas del Sistema Complemento/inmunología , Enfermedad de Crohn/inmunología , Síndromes de Inmunodeficiencia/congénito , Síndromes de Inmunodeficiencia/complicaciones , Animales , Linfocitos B/inmunología , Colitis Ulcerosa/genética , Proteínas del Sistema Complemento/genética , Enfermedad de Crohn/genética , Susceptibilidad a Enfermedades , Humanos , Ratones , Linfocitos T/inmunologíaRESUMEN
Human immunodeficiency virus type 1 can generally use CCR3 and CCR5 for cell entry. We show that envelopes with novel phenotypes arise during "coreceptor switch": one loses the ability to use CCR3 (R5-only phenotype), and another gains use of CXCR4 in addition to CCR5 and CCR3 (R3/R5/X4-using phenotype). The envelope determinants for CCR3 use mapped to three amino acids. One, N356 in conserved region 3, is a potential glycosylation site and has not previously been associated with coreceptor use. The other two, R440 and N448 in conserved region 4, are proximal to but distinct from residues already identified as being important for CCR5 binding.