Table 1.
Possible and existing clustering strategies with clinical implication in IBD.
| Feature | Clustering strategies or suggested clustering strategies with clinical implication |
|---|---|
| Clinical | Montreal classification |
| Increased risk of colectomy, colorectal cancer, and death in PSC-IBD patients compared with non-PSC-IBD patients8 | |
| Genetics | At least four gene loci have been associated with prognosis in CD35 |
| NOD2 risk allele is associated with phenotype of ileitis and absence of colitis36 | |
| Variation in IL-6 is associated with phenotype of ileitis36 | |
| A variant of TL4 is associated with a risk of surgery at disease onset in CD36 | |
| Microbiota | Increase in Bifidobacterium, Collinsella, Lachnospira, Lachnospiraceae, Roseburia, and Eggerthella taxa and reduction in Phascolarctobacterium in CD anti-TNFα responders compared with non-responders61 |
| Increase in Faecalibacterium prausnitzii in UC and CD anti-TNFα responders compared with non-responders62,84 | |
| Increased Eggerthella, Clostridiales, and Oscillospira in CD patients with more quiescent disease and increase in Enterobacteriaceae, Enterobacteriaceae, and Klebsiella in those with more aggressive disease61 | |
| Altered microbial profile is linked to disease recurrence 1 year after ileocaecal resection in CD64 | |
| Lower abundance of Faecalibacterium prausnitzii in CD at the time of ileal resection associated with endoscopic recurrence at 6 months65 | |
| Lower abundance of Faecalibacterium prausnitzii in CD at the time of infliximab cessation associated with quicker relapse63 | |
| Immune system | Frequency of NKp44+ILC3 correlates with disease severity98 |
| Increase of TREG with increasing disease activity in UC and CD101,102 | |
| Greater accumulation of TREG in ileal mucosa in paediatric ileal CD patients compared with adult ileal CD patients, possibly contributing to relative rareness of isolated ileal enteritis in paediatric CD patients103 | |
| Variation in IL-22BP produced by CD4 T cells in association with response to anti-TNF response122 | |
| A subset of ileal CD patients has distinct cellular profile in their inflamed ileum, with accumulation of IgG plasma cells, inflammatory mononuclear phagocytes, activated T cells, and stromal cells, which predicts response to anti-TNF treatment138 | |
| Increase in inflammatory fibroblasts and monocytes as well as DC2 subsets in UC patients predicts non-response to anti-TNF treatment139,140 | |
| Transcriptomics | Transcriptional risk score based on eQTLs data can predict development of stricturing and/or penetrating disease within 3 years from disease onset in paediatric CD34 |
| Upregulation of extracellular matrix accumulation-associated genes in ileum in paediatric CD patients who later developed stricturing disease behaviour131 | |
| Upregulation of genes associated with acute microbial immune responses in paediatric patients who later developed penetrating disease131 | |
| A transcriptional signature based on 17 genes in whole- blood samples from IBD patients can predict aggressive disease course132 | |
| High pre-treatment levels of OSM predict poor response to anti-TNF treatment137 | |
| Rectal transcriptomic profiles UC1 and UC2 predict response to anti-TNF therapy143 |
IBD, inflammatory bowel disease; PSC, primary sclerosing cholangitis; CD, Crohn’s disease; UC, ulcerative colitis IL, interleukin; ILC, innate lymphoid cell; NK, natural killer; TREG, regulatory T cell; BP, binding protein; TNF, tumour necrosis factor; Ig, Immunoglobulin; TLR, Toll-like receptor; OSM, oncostatin M; NOD2, nucleotide-binding oligomerisation domain-containing protein 2; eQTL, expression quantitative trait loci study.