Related IgA1 and IgG producing cells in blood and diseased mucosa in ulcerative colitis

Background: Ulcerative colitis (UC) is a chronic inflammatory bowel disease in which the colonic mucosa is infiltrated with plasma cells producing IgG autoantibodies. It is not known whether this represents a local mucosal response which has switched to IgG or a peripheral response which may have be...

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Bibliographic Details
Published in:	Gut Vol. 51; no. 1; pp. 44 - 50
Main Authors:	Thoree, V C, Golby, S J C, Boursier, L, Hackett, M, Dunn-Walters, D K, Sanderson, J D, Spencer, J
Format:	Journal Article
Language:	English
Published:	London BMJ Publishing Group Ltd and British Society of Gastroenterology 01-07-2002 BMJ BMJ Publishing Group Ltd BMJ Publishing Group LTD Copyright 2002 by Gut
Subjects:	Analysis Antibody-Producing Cells - immunology Antigens Base Sequence Bias Biological and medical sciences CDR Clone Cells Colitis, Ulcerative - blood Colitis, Ulcerative - immunology Colitis, Ulcerative - pathology Colon Colon - immunology Colon - pathology complementarity determining region Female Gastroenterology. Liver. Pancreas. Abdomen Humans IgA IgG Immunoglobulin A, Secretory - biosynthesis Immunoglobulin A, Secretory - genetics Immunoglobulin G - biosynthesis Immunoglobulin G - genetics immunoglobulin genes Immunoglobulins Inflammation Inflammatory Bowel Disease Intestinal mucosa Intestinal Mucosa - immunology Intestinal Mucosa - pathology Male Medical sciences Middle Aged Molecular Sequence Data Mutation Other diseases. Semiology Pathogenesis PBL PCR peripheral blood lymphocytes Physiological aspects plasma cells Polymerase chain reaction reverse transcription-PCR RT-PCR Sequence Alignment Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Studies Ulcerative colitis United Kingdom Human IgA Leukocyte Pathogenesis Mucosa Autoantibody IgG Biosynthesis Blood Inflammatory disease Digestive diseases Intestinal disease Infiltration Colon Ulcerative colitis
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Summary:	Background: Ulcerative colitis (UC) is a chronic inflammatory bowel disease in which the colonic mucosa is infiltrated with plasma cells producing IgG autoantibodies. It is not known whether this represents a local mucosal response which has switched to IgG or a peripheral response which may have been initiated by peripheral antigen which homed to the colonic mucosa. The clonal distribution of IgG secreting cells and isotype switched variants in UC is not known. Aims: To investigate the clonal distribution of mucosal IgG in UC and to search for related IgG and IgA secreting cells in normal and diseased mucosa and blood in UC. To investigate characteristics which may discriminate between the mucosal and peripheral repertoire in the normal mucosa and in UC. Patients: Blood and normal and diseased mucosa from two patients with UC were studied. Methods: Immunoglobulin gene analysis and clone specific polymerase chain reaction were used to study the clonal distribution and characteristics of IgG and related IgA in the mucosa and blood of patients with UC. Results: The IgG response in the mucosa of UC patients included widespread clones of cells that were present in both the diseased mucosa and blood but that were scarce in normal mucosa. Clonally related IgA class switch variants, all IgA1, were detected but also only in the diseased mucosa and blood. This suggests that these clones home preferentially to the diseased mucosa. We showed that JH1 usage was characteristic of the peripheral repertoire, and that examples of JH1 usage were observed in mucosal IgG in UC. Conclusions: Overall, these data are consistent with a model of UC in which a peripheral response is expressed and expanded in the colonic mucosa.
Bibliography:	istex:FFBE6274DDD800F143A96442D230F36500AF7A68 ark:/67375/NVC-FT5QVP55-T Correspondence to:  J Spencer, Department of Histopathology, GKT Medical School, Lambeth Palace Rd, London SE1 7EH, UK;  jo.spencer@kcl.ac.uk href:gutjnl-51-44.pdf local:0510044 PMID:12077090 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Correspondence to: J Spencer, Department of Histopathology, GKT Medical School, Lambeth Palace Rd, London SE1 7EH, UK; jo.spencer@kcl.ac.uk
ISSN:	0017-5749 1468-3288 1458-3288
DOI:	10.1136/gut.51.1.44