Figure 2.

Examples of heterogeneity between UC, CD and healthy subjects. The first row illustrates how in UC all the DCs have decreased capacity to produce RA [green DCs] compared with healthy individuals [white DCs], whereas DCs from CD patients show heterogeneity in their RA production capacity.⁸⁴ The second row illustrates that in early CD the abundance of colonic ILC1s is selectively increased, whereas in early UC the abundance of ILC2s is increased.⁹⁸ Later in the disease course, ILC1s and ILC2s are increased compared with healthy individuals in both disease groups.⁹⁸ The third row shows an example of microbiota-based clustering, where CD patients responding to anti-TNF treatment have increased abundance of Bifidobacterium, Collinsella, Lachnospira, Lachnospiraceae, Roseburia, and Eggerthella taxa and reduction in Phascolarctobacterium compared with anti-TNFα non-responders, whereas UC patients do not seem to show clustering based on these bacteria and anti-TNF response.⁶¹ The fourth row exemplifies a possible clustering strategy based on CD49b⁺LAG-3⁺ IL-10-producing type 1 TREG cells that show more variable frequencies in UC compared with CD.⁸⁵ The fifth row illustrates that UC patients with PSC have higher abundance of colonic ILCs compared with UC patients without PSC.⁹⁶ CD, Crohn’s disease; UC, ulcerative colitis; IL, interleukin; Th, T helper cell; ILC, innate lymphoid cell; DC, dendritic cell; RA, retinoic acid; TNF, tumour necrosis factor; PSC, primary sclerosing cholangitis.