Expression of Toll-like receptor-3 is enhanced in active inflammatory bowel disease and mediates the excessive release of lipocalin 2
Version of Record online: 6 AUG 2013
© 2013 British Society for Immunology
Clinical & Experimental Immunology
Volume 173, Issue 3, pages 502–511, September 2013
How to Cite
Østvik, A. E., Granlund, A. v. B., Torp, S. H., Flatberg, A., Beisvåg, V., Waldum, H. L., Flo, T. H., Espevik, T., Damås, J. K. and Sandvik, A. K. (2013), Expression of Toll-like receptor-3 is enhanced in active inflammatory bowel disease and mediates the excessive release of lipocalin 2. Clinical & Experimental Immunology, 173: 502–511. doi: 10.1111/cei.12136
- Issue online: 6 AUG 2013
- Version of Record online: 6 AUG 2013
- Accepted manuscript online: 14 MAY 2013 03:25AM EST
- Manuscript Accepted: 8 MAY 2013
- Liaison Committee between the Central Norway Regional Health Authority and NTNU
- Norwegian Cancer Society
- Liaison Committee between St Olav's University Hospital and the Faculty of Medicine, NTNU
Fig. S1. Immunohistochemical staining of Toll-like receptor (TLR)-3 in colonic biopsy from actively inflamed mucosa in ulcerative colitis and three different types of negative controls in the same experiment are shown. We used serial sections from same biopsy. The first negative control was made by omitting primary antibody (no ab). In the second negative control, primary antibody was replaced by isotype immunoglobulin (Ig)G1 directed against non-human epitope (IgG1). The third control was made by blocking primary antibody with recombinant human TLR-3 peptide (rhTLR-3+TLR-3ab); ×10 and ×40 magnification for each slide are shown.
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