Back

IL-1-driven stromal-neutrophil interaction in deep ulcers defines a pathotype of therapy non-responsive inflammatory bowel disease

Friedrich, M.; Pohin, M.; Jackson, M. A.; Korsunsky, I.; Bullers, S.; Rue-Albrecht, K.; Christoforidou, Z.; Santhananthan, D.; Ravindran, R.; Sanches Peres, R.; Sharpe, H.; Wei, K.; Watts, G. F. M.; Mann, E. H.; Geremia, A.; Thomas, T.; Attar, M.; Oxford IBD Cohort Investigators, ; Roche Fibroblast Network Consortium, ; McCuaig, S.; Thomas, L.; Collantes, E.; Uhlig, H. H.; Sansom, S. N.; Easton, A.; Raychaudhuri, S.; Travis, S. P.; Powrie, F. M.

2021-02-06 immunology
10.1101/2021.02.05.429804 bioRxiv
Show abstract

Current inflammatory bowel disease (IBD) therapies are ineffective in a high proportion of patients. Combining bulk and single-cell transcriptomics, quantitative histopathology, and in situ localisation, we describe heterogeneity of the tissular inflammatory response in IBD treatment failure. Among inflammatory pathotypes, we found high neutrophil infiltration, activation of fibroblasts, and vascular remodelling at sites of deep ulceration was a feature of non-response to several anti-inflammatory therapies. Activated fibroblasts in the ulcer bed display neutrophil chemoattractant properties that are IL-1R- but not TNF-dependent. The identification of distinct, localised, tissular pathotypes associated with treatment non-response will aid precision targeting of current therapeutics and provide a biological rationale for IL-1 signalling blockade in ulcerating disease.

Matching journals

The top 5 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.