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. 2018 Jun 1;9:1212. doi: 10.3389/fimmu.2018.01212

Table 1.

Models of Th cell-driven inflammatory bowel disease.

Mouse model Type of model Th-type/s involved Key cytokines/TFs Reference
DSS colitis Chemical Th1 (Acute) IFN-γ, TNF, T-bet (13, 15, 2022)
Th2 (Chronic) IL-4, IL-13, STAT6, GATA3
Th9 IL-9, PU.1

TNBS colitis Chemical Th1 (Acute) TNF, T-bet (2330)
Th2 (Chronic) IL-13, GATA3
Th9 (Acute) IL-9, PU.1
Th17 (Acute) IL-17R, SMAD7

Oxazolone Chemical Th2, NK-T IL-4, IL-13 (29, 3135)
Th9 IL-9, GATA3
Th17 TGF-β, SMAD7

Anti-CD40 Chemical (activating antibody) Th1 IL-12 (36)
Th17 IL-17, IL-23

Citrobacter rodentium Infectious Th1 IFN- γ (37, 38)
Th17 IL-17A, IL-17F

RAG or SCID T cell transfer model Transfer Th1 IFN-γ, STAT4, T-bet (1416, 23, 3941)
Th17 IL-23, STAT3, SMAD2

Abcb1an−/− Transgenic Th17 IL-23 (42)

Tcrα−/− Transgenic Th2-like IL-4 (43)

Il10/Il10r−/− Transgenic Th17 IL-17, IL-23 (44)

Th-association was determined by induced expression in a particular model or by mechanistic studies, where cytokines/TFs were manipulated by gene deletion or blocking antibody.

Acute, acute exposure to chemical; Chronic, repeating exposure to chemical; STAT, signal transducer and activator of transcription; IL, interleukin; TNF, tumor necrosis factor; IFN, interferon; TFs, transcription factors.