Key result
Transferring IFN-gamma knockout CD4+ T cells fails to induce wasting disease, demonstrating IFN-gamma's essential role.
Why the study?
Does the transfer of CD45RBhigh CD4+ T cells from IFN-gamma knockout mice prevent wasting disease in congenic SCID mice compared to cells from normal mice?
Does the transfer of CD45RBhigh CD4+ T cells from IFN-gamma knockout mice prevent wasting disease in congenic SCID mice compared to cells from normal mice?
IFN-gamma plays an essential and non-redundant role in the pathogenesis of wasting disease in a murine model of inflammatory bowel disease.
Does not support IFN-gamma modulation in human IBD yet; leaves open translation from this murine colitis model.
Transfer of CD45RBhigh CD4+ T cells from normal mice to congenic SCID mice induces wasting disease, a murine model of inflammatory bowel disease. In this model, colonic inflammation is considered to be caused by a disregulated Th1 response, and Th1 cytokines, especially IFN-gamma, have been suggested to play an important role in the pathogenesis of wasting disease. In order to elucidate the potential role of IFN-gamma in the pathogenesis of wasting disease, we transferred CD45RBhigh CD4+ T cells from IFN-gamma knockout (GKO) mice to congenic SCID mice. The recipient mice were absolutely free of symptoms and clinical signs of disease and showed body-weight gain similar to that seen in normal mice. These data demonstrate the essential and non-redundant role of IFN-gamma in the pathogenesis of wasting disease.
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Ito et al. (1997) studied Wasting disease (murine model of inflammatory bowel disease). Transfer of CD45RBhigh CD4+ T cells from IFN-gamma knockout (GKO) mice vs. Transfer of CD45RBhigh CD4+ T cells from normal mice was evaluated on Wasting disease symptoms, clinical signs, and body-weight gain. Transfer of CD45RBhigh CD4+ T cells from IFN-gamma knockout mice to SCID mice did not induce wasting disease, demonstrating the essential role of IFN-gamma in its pathogenesis.
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