These mice display increased GC formation and perturbed post-GC differentiation characterized by a decreased number of post-isotype switch plasma cells.
Moreover, LPS stimulation of CD19+ cells isolated from these mice display increased proliferation, augmented AKT and NFκB activation as well as increased expression of c-myc and cyclinD1.
We show that transgenic mice display increased transepidermal water loss and elevated skin pH, abnormal stratum corneum lipids, focal epidermal hyperplasia, activated keratinocytes expressing more thymic stromal lymphopoietin, a T helper type 2/T helper type 17 skin immune response, and increased serum IgE.
Abcg1-deficient mice display increased thymocyte cellularity and enhanced proliferation of thymocytes and peripheral T lymphocytes in vivo.
Initially, Cdk5 KO mice display increased NMDAR-mediated currents, enhanced plasticity, and impaired neuronal repolarization.
Similarly, transcription factor A (Tfam) knockout mice display increased gene expression of several glycolytic enzymes [46].
The immature pro-B cells from LEF-1 deficient mice display increased sensitivity to apoptosis [29], although the exact mechanism is unclear.
In agreement with our results, CB1 [26] and CB2 [27] receptor knock-out mice display increased behavioral sensitivity in various models of pain.
β-cells from Hq mutant mice display increased sensitivity to hydrogen peroxide-induced apoptosis, which was confirmed in human islets in which AIF was depleted by siRNA.
TRAIL deficient mice display increased susceptibility to carcinogen induced tumorigenesis and have increased metastatic potential [19], [20], demonstrating that TRAIL exerts tumor suppressor activity, and suggests an important role of endogenous TRAIL in tumor surveillance.
Therefore increased anxiety should not be generally interpreted as a model for psychiatric pathology, e.g. wild mice display increased anxiety behavior in response to open areas compared to inbred laboratory strains [30].
