🔍 WHY IS IT USEFUL?
The T cell-induced colitis model reproduces many of the clinicopathological features observed in IBD. A major advantage of this model is its usefulness in the study of immunological mechanisms underlying chronic intestinal inflammation. It can also be used to evaluate the role of different lymphocyte populations, cytokines, and proteins expressed during the onset and progression of the disease.

🔍 HOW DOES THE MODEL WORK?
In detail, the adoptive transfer of CD4⁺ naive CD45RB^high cells (naive cells lacking the regulatory T cell population, Treg) from healthy wild-type mice into syngeneic recipient mice lacking T and B cells (e.g., RAG knockout mice) induces extensive colitis and small intestinal inflammation after about 5–8 weeks following the transfer.1–3

In contrast, control mice that receive CD4⁺ CD45RB^low cells (a population containing Tregs) do not develop colitis: the mice remain healthy, and no T cell activation is observed in the lamina propria.

The duration of the model is about 2 months, during which mice clinically exhibit weight loss, loose stools, and diarrhea, reproducing typical symptoms of the human disease.

From a histopathological perspective, the distal colon of mice with active disease shows:

Erosions and hyperplasia of the epithelial barrier, and transmural inflammation with massive immune cell infiltration — all features that closely resemble those seen in patients with IBD.