%0 Journal Article
%T B Lymphocyte intestinal homing in inflammatory bowel disease
%A Caterina Defendenti
%A Piercarlo Sarzi-Puttini
%A Silvia Grosso
%A Annamaria Croce
%A Olivia Senesi
%A Simone Saibeni
%A Simona Bollani
%A Piero Almasio
%A Savino Bruno
%A Fabiola Atzeni
%J BMC Immunology
%D 2011
%I BioMed Central
%R 10.1186/1471-2172-12-71
%X 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, ¦Ë and ¦Ê 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¡À 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
%K Inflammatory bowel disease
%K inflammation
%K mucosal immunity
%K lymphocytes
%K B1 cells
%K lymphocyte homing
%U http://www.biomedcentral.com/1471-2172/12/71