Accessory cells in Crohn's disease of the terminal ileum.
We present a study which describes the immunophenotype and distribution of accessory cells in 13 resections of terminal ileum from patients with Crohn's disease. A panel of antibodies working in paraffin-embedded tissue was employed and these included PGM1 (CD68), S-100 protein, WR18 (HLA class II), factor XIIIa and acid cysteine proteinase inhibitor. This study revealed a heterogeneity of accessory cell populations which was profoundly influenced by local inflammatory and repair mechanisms. Both acid cysteine proteinase activity and S-100 protein positive cells are identified in more actively inflamed areas. The acid cysteine proteinase activity positive dendritic cell population was particularly numerous in ulcer bases. S-100 protein positive dendritic cells had a more limited distribution in close proximity to the epithelium in inflamed but otherwise intact mucosa adjacent to the areas of ulceration. PGM1 revealed normal distribution of macrophages within histologically uninvolved areas and, in addition, also stained granulomas and large numbers of dendritic cells in the inflamed, ulcerated and scarred areas. Factor XIIIa positive dendritic cells were especially numerous in areas of active scarring where they co-localized with PGM1 positive cells. They were largely absent from the more superficial ulcerated areas. HLA class II was strongly expressed on mononuclear inflammatory and dendritic cells. The strength of epithelial staining for HLA class II reflected the intensity of adjacent inflammation, except on ulcer-associated epithelium which consistently showed up-regulation independent of the severity of the inflammatory process. This study shows that localized alterations in the accessory cell distribution in Crohn's disease correlate with different states in the evolution of the inflammatory and repair process of the disease. The more acute lesions are associated with recruitment of acid cysteine proteinase activity and S-100 protein positive dendritic cells while factor XIIIa stained dentritic cells are especially numerous in areas of scarring.
Sarsfield
P
P
University Department of Pathology, Southampton General Hospital, UK.
Jones
D B
DB
Wright
D H
DH
D000938:Antigen-Presenting Cells / Q000473:pathology*; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D003424:Crohn Disease / Q000276:immunology* / Q000473:pathology*; D015853:Cysteine Proteinase Inhibitors / Q000032:analysis; D000949:Histocompatibility Antigens Class II / Q000032:analysis; D006801:Humans; D007082:Ileum / Q000276:immunology* / Q000473:pathology*; D007150:Immunohistochemistry; D009418:S100 Proteins / Q000032:analysis; D011503:Transglutaminases / Q000032:analysis; D000097382:CD68 Molecule
D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D015853:Cysteine Proteinase Inhibitors; D000949:Histocompatibility Antigens Class II; D009418:S100 Proteins; D011503:Transglutaminases; C067980:CD68 antigen, human; D000097382:CD68 Molecule