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Updated: Jul 13, 2026
Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
Published on: April 21, 2015
CD2 deficiency partially prevents small bowel inflammation and improves parasite control in murine Toxoplasma gondii
Nina-N Pawlowski1, Daniela Struck, Katja Grollich
1Medizinische Klinik I, St. Charité-Universitätsmedizin Berlin, Berlin, Germany.
Aim:
To investigate whether bowel inflammation and/or parasite control is altered in the absence of the T cell adhesion molecule CD2.
Methods:
Wildtype (WT) and CD2 deficient (CD2(-/-)) mice were infected with 100 cysts of Toxoplasma gondii (T. gondii) (ME49) by gavage. On d 7 after infection mice were killed. Necrosis and the number of parasites/cm ileum were determined. Cytokine levels of stimulated cells as well as sera were evaluated. Secondly, survival of WT vs CD2(-/-) mice was analysed using Kaplan-Meier analysis.
Results:
CD2(-/-) mice survived longer than WT mice (mean: 23.5 vs 7.1 d, P = 0.001). Further, CD2(-/-) mice showed less weight loss and less ileal inflammation than WT mice at d 7 post infection. In addition, the number of parasites in the ileum was significantly lower in CD2(-/-) mice than in WT mice (88 +/- 12 vs 349 +/- 58 cm, P < 0.01). This was paralleled by lower production of IFN-gamma and IL-6 from TLA-stimulated mLN cells and increased IFN-gamma production by splenocytes.
Conclusion:
CD2 deficient mice are more resistant to T. gondii infection than WT mice. In contrast to most current immunosuppressive or biological therapies CD2 deficiency reduces intestinal inflammation and at the same time helps to control infection.
Insights
Mice lacking the T cell adhesion molecule CD2 showed increased resistance to Toxoplasma gondii infection. CD2 deficiency reduced intestinal inflammation and parasite load, offering a potential therapeutic avenue.
Area of Science:
- Immunology
- Parasitology
- Infectious Diseases
Background:
- T cell adhesion molecule CD2 plays a role in immune responses.
- Toxoplasma gondii infection causes significant intestinal inflammation and morbidity.
Purpose of the Study:
- To determine the role of CD2 in host defense against Toxoplasma gondii.
- To investigate the impact of CD2 deficiency on intestinal inflammation and parasite control.
Main Methods:
- Wildtype and CD2-deficient mice were infected with T. gondii.
- Evaluated ileal inflammation, parasite burden, cytokine profiles, and survival rates.
Main Results:
- CD2-deficient mice exhibited prolonged survival and reduced weight loss.
- Lower parasite numbers and decreased ileal inflammation were observed in CD2-deficient mice.
- Altered cytokine production (IFN-gamma, IL-6) was noted in CD2-deficient mice.
Conclusions:
- CD2 deficiency confers enhanced resistance to T. gondii infection.
- CD2 deficiency simultaneously reduces intestinal inflammation and controls parasite infection.
- Targeting CD2 may offer a novel therapeutic strategy for toxoplasmosis.
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