TY -的T1 -遗传inflamm之间的共性atory bowel disease and sarcoidosis: the beginning of the end or the end of the beginning? JF - European Respiratory Journal JO - Eur Respir J SP - 489 LP - 491 DO - 10.1183/09031936.00160310 VL - 37 IS - 3 AU - Cerri, S. AU - du Bois, R.M. AU - Spagnolo, P. Y1 - 2011/03/01 UR - //www.qdcxjkg.com/content/37/3/489.abstract N2 - Crohn's disease (CD) and ulcerative colitis, collectively known as inflammatory bowel disease (IBD), and sarcoidosis are multifactorial disorders thought to result from complex interactions between environmental stimuli (e.g. infectious agents), susceptibility genes (which may predispose to the development of granulomatous inflammation) and modifier genes (which may affect disease phenotype in people already susceptible). Neither IBD nor sarcoidosis is the result of defects in a single major gene or chemical pathway; instead, multiple genes, each contributing a relatively minor effect, are likely to be involved. In addition to the granulomatous histopathology, both diseases share a number of similarities in terms of ocular, dermatological and joint manifestations, although sarcoidosis rarely involves the gastrointestinal tract and IBD rarely involves the lung. Immunological, bacteriological and genetic data support a link between CD and sarcoidosis. Both disorders share a similar, yet distinct, immune response, histologically defined by non-caseating granulomas. Up to 50% of patients with CD have been reported to test positive for Kveim antigens, although these data are not replicated in all studies 1. Mycobacteria have been detected in intestinal tissue of patients with CD and in the lungs of patients with sarcoidosis 2, 3. A CD4/CD8 lymphocyte ratio >3.5 on bronchoalveolar lavage (BAL) is commonly observed in sarcoidosis, often preceding granuloma formation 4, with a similar expansion of T-cell subsets demonstrated in the lungs of patients with CD 5. CD4 lymphocytes are activated in the intestinal mucosa of patients with CD, suggesting a cell-mediated disease mechanism in the gut similar to that displayed in pulmonary sarcoidosis. Furthermore, both in sarcoidosis and CD the concept of a genetic component is supported by disease being more common in monozygotic twins compared with dizygotic twins. In contrast with these similarities, tuberculin anergy, salivary gland involvement, the classical lymph and salivary gland … ER -