Skin- and gut-homing molecules on human circulating γδ T cells and their dysregulation in inflammatory bowel disease.
| Autor: | Mann ER; Antigen Presentation Research Group, Imperial College London, Northwick Park and St Mark’s Campus, Level 7W, St Mark’s Hospital,Watford Road, Harrow HA1 3UJ, UK., McCarthy NE, Peake ST, Milestone AN, Al-Hassi HO, Bernardo D, Tee CT, Landy J, Pitcher MC, Cochrane SA, Hart AL, Stagg AJ, Knight SC |
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| Jazyk: | angličtina |
| Zdroj: | Clinical and experimental immunology [Clin Exp Immunol] 2012 Nov; Vol. 170 (2), pp. 122-30. |
| DOI: | 10.1111/j.1365-2249.2012.04649.x |
| Abstrakt: | Changes in phenotype and function of γδ T cells have been reported in inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC). Dysregulation of lymphocyte migration plays a key role in IBD pathogenesis; however, data on migratory properties of γδ T cells are scarce. Human circulating γδ T cells from healthy controls (n = 27), patients with active CD (n = 15), active UC (n = 14) or cutaneous manifestations of IBD (n = 2) were characterized by flow cytometry. Circulating γδ T cells in healthy controls were CD3(hi) and expressed CD45RO. They expressed gut-homing molecule β7 but not gut-homing molecule corresponding chemokine receptors (CCR)9, or skin-homing molecules cutaneous lymphocyte-associated antigen (CLA) and CCR4, despite conventional T cells containing populations expressing these molecules. CCR9 expression was increased on γδ T cells in CD and UC, while skin-homing CLA was expressed aberrantly on γδ T cells in patients with cutaneous manifestations of IBD. Lower levels of CD3 expression were found on γδ T cells in CD but not in UC, and a lower proportion of γδ T cells expressed CD45RO in CD and UC. Enhanced expression of gut-homing molecules on circulating γδ T cells in IBD and skin-homing molecules in cutaneous manifestations of IBD may be of clinical relevance. (© 2012 The Authors. Clinical and Experimental Immunology © 2012 British Society for Immunology.) |
| Databáze: | MEDLINE |
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