title: T-cell co-stimulatory molecules are upregulated on intestinal macrophages from inflammatory bowel disease mucosa.
abstract: OBJECTIVE
  Macrophages play an important role during mucosal inflammation in inflammatory bowel disease (IBD). As the co-stimulatory molecules B7-1 (CD80) and B7-2 (CD86) play an integral role in the activation of T cells by antigen-presenting cells (APC) we investigated the surface expression of B7-1 and B7-2 on colonic macrophages from normal and IBD mucosa.
  
  
  METHODS
  Intestinal macrophages were isolated from biopsies of 13 control persons and 14 patients with IBD (seven with Crohn's disease (CD); and seven with ulcerative colitis (UC)). Cells were characterized by triple fluorescence flow cytometrical analysis using CD33 as macrophage marker.
  
  
  RESULTS
  The expression of B7-1 (CD80) (9.2% +/- 4.2%) and B7-2 (CD86) (15.1% +/- 7.3%) was low on colonic macrophages from normal mucosa, indicating only a low antigen presenting potential. However, on macrophages from IBD colon there was a significant increase in the expression of co-stimulatory molecules (CD80, 33.8% +/- 8.9%, P = 0.00005 vs. control; CD86, 39.9% +/- 8.8%, P = 0.00002). There was no significant difference between CD and UC in the expression of CD80 (CD, 31.3% +/- 6.7%; UC, 34.4% +/- 13.3%) and CD86 (CD, 41.9% +/- 3.8%; UC, 35.6% +/- 13.8%). While in normal mucosa only 10.6% +/- 4.9% of the macrophages expressed CD14, more than 90% of the CD86/CD80 positive cells of the inflamed mucosa were positive for CD14.
  
  
  CONCLUSIONS
  Colonic macrophages from normal mucosa rarely express the co-stimulatory molecules CD80 and CD86. In IBD a new macrophage population is found with high expression of co-stimulatory molecules presumably responsible for the perpetuated immune response.
authors.affiliation: Department of Internal Medicine I, University of Regensburg, Germany. gerhard.rogler@klinik.uni-regensburg.de
authors.forename: G
authors.initials: G
authors.lastname: Rogler
authors.forename: M
authors.initials: M
authors.lastname: Hausmann
authors.forename: T
authors.initials: T
authors.lastname: Spöttl
authors.forename: D
authors.initials: D
authors.lastname: Vogl
authors.forename: E
authors.initials: E
authors.lastname: Aschenbrenner
authors.forename: T
authors.initials: T
authors.lastname: Andus
authors.forename: W
authors.initials: W
authors.lastname: Falk
authors.forename: J
authors.initials: J
authors.lastname: Schölmerich
authors.forename: V
authors.initials: V
authors.lastname: Gross
mesh_terms: D015703:Antigens, CD / Q000096:biosynthesis*; D015214:Antigens, Differentiation, Myelomonocytic / Q000096:biosynthesis; D018122:B7-1 Antigen / Q000096:biosynthesis*; D051940:B7-2 Antigen; D002452:Cell Count; D002454:Cell Differentiation; D002478:Cells, Cultured; D003713:Dendritic Cells / Q000166:cytology / Q000276:immunology; D005434:Flow Cytometry; D006801:Humans; D007249:Inflammation / Q000276:immunology; D015212:Inflammatory Bowel Diseases / Q000276:immunology*; D007413:Intestinal Mucosa / Q000276:immunology*; D018950:Lipopolysaccharide Receptors / Q000096:biosynthesis; D008264:Macrophages / Q000166:cytology / Q000276:immunology*; D008562:Membrane Glycoproteins / Q000096:biosynthesis*; D017452:Receptors, IgG / Q000096:biosynthesis; D063268:Sialic Acid Binding Ig-like Lectin 3; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D018122:B7-1 Antigen; D051940:B7-2 Antigen; C571163:CD33 protein, human; C497964:CD86 protein, human; D018950:Lipopolysaccharide Receptors; D008562:Membrane Glycoproteins; D017452:Receptors, IgG; D063268:Sialic Acid Binding Ig-like Lectin 3