It is reasonable to expect that mice with specific inactivation of Smad4 in T cells phenotypically resemble T-cell-specific TGF- βR-deficient mice and develop autoimmunity.
These mice are similar to Tg197 mice and develop a spontaneous arthritis at from 8to1010 weeks of age [ 15].
In experimental animal models, mice that lack p27 protein expression are larger than wild-type mice and develop large organs and pituitary tumours, most probably resulting from uncontrolled cell proliferation [ 24- 26].
These double-transgenics are present on the genetic background of C57BL/6 mice and develop an EAE-like neurological syndrome described as "spontaneous opticospinal encephalomyelitis (OSE)" 30 or "Devic-like disease" 6.
Mice that over-express COX-2 in basal epidermal cells, through keratin 5 promoters, are significantly more susceptible to genotoxic carcinogens than wild-type mice, and develop epidermal hyperplasia and dysplasia after single epicutaneous applications of 0.5 μM DMBA in 0.1 ml acetone [ 85].
Therefore, we hypothesized that a low but sufficient level of sympathetic activation may maintain a low level of the inflammation state in the L5 cord to accumulate MHC class II+CD11b+ cells in the L5 cord of EAE-recovered mice and develop EAE relapse after pain induction.
