CD2 deficiency partially prevents small bowel inflammation and improves parasite control in murine Toxoplasma gondii infection.

Abstract

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.