| Mouse models | Effects of ablation of specific adaptive immune components on C. rodentium infection | Refs |
| Mice lacking CD4+ T cells or TCRαβ+ T cells | A survival limit of two weeks and exhibited 100% mortality | [59] [64] |
| Mice lacking CD8+ T cells or TCRγδ+ T cells | Do not adversely affect survival of infection | [59] |
| Mice without mature B cells (μMT mice) | Cannot lessen bacterial load or clear bacterial colonization over a prolonged period | [63] [65] [66] |
| RAG1-deficient mice (both B and T cells are absent) | Develop chronic intestinal colonization and unable to clear infection and die after 3-4 weeks | [59] [63] [67] |
| IgA- and IgM- deficient mice | Develop effective immunity against a secondary challenge and play a negligible role in controlling C. rodentium infection. | [65] |
| Mice deficient in IgG antibodies | Lose the ability to develop protective response against secondary challenge. | [65] |
| IFNγ-deficient mice | Higher bacterial numbers and enhanced mucosal thickening in colons and cannot clear infection until day 28 | [68] |
| IL-12 deficient mice | Elicit higher bacterial numbers for the first 3 weeks of infection and eventually clear infection by day 35 | [30] |
| Mice lacking IL-22 | Display systemic bacterial load and enhanced epithelial hyperplasia and mortality range up to 100% within the first two weeks of infection | [69] |
| Treg deficient mice (DEREG mice) | Diminished bacterial clearance, systemic dissemination of bacteria with compromised Th17 immune response accompanied by less inflammation-associated pathology | [70] |
| IL-10 ablated mice | Resolve infection earlier than wild-type mice with less infection associated colitis | [71] |