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| Immune cell | Physiological functions in the intestinal tract | The pathophysiological role in IBD |
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| Macrophages | Assist Treg cells’ expansion and production of IL-10 [21, 22]. | Secretion of large amounts of pro-inflammatory cytokines such as IL-23 and TNF-α [29, 30]. |
| ILCs | Controlling tissue homeostasis [34, 35]. | ILC1 can release IFN-γ [36, 37, 41]; LC2 can produce IL-5 and IL-13 cytokines [40]; patients with IBD express ILC3 genes (IL17A, IL22, and IL23R) [44]. |
| NKT cells | Response to infectious pathogens, prevention of autoimmune diseases, and maintenance of self-tolerance [57]. | NKT cells are sources of IL-13 [60]. The expression of IL-13 was significantly increased in UC [60, 61]. |
| IECs | Defend against intestinal luminal bacteria and pathogen-associated molecular patterns [64]. | TLR5 recognizes flagellin, whose activation stimulates the NF-κB, which induces the secretion of chemokines IL-8 and MIP3 [67, 68]. ISG15 expression was increased and ISG15 could enhance IL-12-induced IFN-γ release [71, 73, 74]. |
| Th1 cells | Protective immunity against microbial pathogens and tumors [75]. | In CD, Th1 cell responses are associated with an increased expression of IL-12 [79–81]. |
| Th2 cells | Promote antihelminth immunity, suppress type 1-driven autoimmune disease and maintain metabolic homeostasis [88]. | UC is characterized by Th2-related cytokines (IL-5 and IL-13) [60, 61, 95, 96]. |
| Th17 cells | Maintaining symbiotic populations at important barrier sites [99]. | The mucosa of patients with IBD can detect high levels of IL-17A [78, 105, 106], IL-17C [102], and IL-21 [82, 107]. |
| Treg cells | Tregs act as the key regulators of intestinal homeostasis [108, 109]. | Tregs may differentiate into Th17 cells, resulting in the IL-17+ and FoxP3+ subsets of T cells [48]. |
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