Does mCMV infection increase early T-lymphocyte influx in atherosclerotic lesions in apoE knockout mice?
MCMV infection may exacerbate the atherosclerotic process in apoE knockout mice by means of an acute lymphocytic inflammatory response. In contrast to the MCMV induced effect in apoE knockout mice, MCMV infection did not increase the influx of T-lymphocytes in atherosclerotic lesions of C57Bl/6J mice.
The nature of the mutation and its segregation with disease support that it is disease-causing. Previously reported NKX2.1 mutations have been associated with "brain-thyroid-lung" syndrome and a spectrum of more severe pulmonary phenotypes. We conclude that genetic mechanisms may cause NEHI and that NKX2.1 mutations may result in, but are not the predominant cause of, this phenotype. We speculate that altered expression of NKX2.1 target genes other than those in the surfactant system may be responsible for the pulmonary pathophysiology of NEHI.