B Lymphocyte intestinal homing in inflammatory bowel disease

The IPCs in small intestinal, colonic and rectal biopsy specimens of patients with IBD were analysed by means of immunofluorescence using polyclonal rabbit anti-human Ig and goat anti-human IgM. The B cell phenotype of the IPC-positive samples was assessed using monoclonal antibodies specific for CD79, CD20, CD23, CD21, CD5, λ and κ chains. Statistical correlations were sought between the histological findings and clinical expression.The study involved 96 patients (64 with ulcerative colitis and 32 with Crohn's disease). Two different patterns of B lymphocyte infiltrates were found in the intestinal tissue: one was characterised by a strong to moderate stromal localisation of small IgM+/CD79+/CD20-/CD21-/CD23-/CD5± IPCs (42.7% of cases); in the other (57.3%) no such small IPCs were detected in stromal or epithelial tissues. IPCs were significantly less frequent in the patients with Crohn's disease than in those with ulcerative colitis (p = 0.004).Our findings suggest that different immunopathogenetic pathways underlie chronic intestinal inflammation with different clinical expressions. The presence of small B lymphocytes resembling B-1 cells also seemed to be negatively associated with Crohn's disease. It can therefore be inferred that the gut contains an alternative population of B cells that have a regulatory function.Crohn's disease (CD) and ulcerative colitis (UC) are idiopathic inflammatory bowel disorders [1] attributable to an abnormal immune response to bacterial antigens. Deficiencies in anti-inflammatory and immunosuppressive mechanisms are important to the development of the disease, but the basic pathogenetic mechanisms are still largely unknown [2].Recently collated evidence supports the view that IBD consists of disorders with distinct genetic, microbial and environmental determinants that cluster into an UC or CD phenotype [3]. IBD is polygenic, and experimental data suggest that a number of not mutually exclusive pathways may contribute to the inflam