While evidence exists for this paradigm in some mouse models, the proof in human autoimmune diseases is still outstanding.
If all goes well in the mouse models, the researchers plan to pursue tests in human subjects.
With the development of genetically engineered mouse models, the functional consequences and tissue dynamics of genetic alterations can be defined at discrete stages of carcinogenesis.
While the principles of vaccine design can be developed in mouse models, the real operative test is in the clinic, using patients in temporary remission.
After studies in preclinical mouse models, the efficacy and safety of tumor-specific vaccination strategies is currently being evaluated in cancer patients.
In both the Emx1-Cre and Dlx5/6-Cre conditional mouse models the latency to scPTZ-induced seizures was significantly shorter than for their wild-type littermates.
In preclinical mouse models, the Ad vaccines expressing M2e and NP elicit robust NP-specific CD8+ T-cell responses and moderate antibody responses to all three M2e sequences.
In similar mouse models, the fluorescent label eventually disappears, and researchers are unable to assess what happens many months after a mouse first learns something or after a disease has set in.
In early tests in cultured cancer cells and in mouse models, the EZH2 inhibitor reversed the altered pattern of epigenetic marks, restored the activity of the genes silenced by these marks, and slowed the growth of the lymphoma cells (NB my institution was not involved in this study).
In all mouse models, the immunotoxin reduced the numbers of PD-1-expressing cells, of total T cells and of cells of an autoreactive T-cell clone found in inflamed organs, while maintaining active adaptive immunity, as evidenced by full-strength immune responses to vaccinations.
Together with studies in pathophysiologic states and the examination of genetically engineered mouse models, the evolving picture points to important roles for the SLC26 family in health and disease states.
