Altogether, the data collected in this study regarding Treg suppressive function remain inconclusive. Although the present study did not comprise a placebo-group, it delivered valuable new information. We earlier performed a crosssectional study, in which serum 25D levels correlated with peripheral T cell homeostasis. However, the cross-sectional design did not allow statements on causality, since physical exercise and UV exposure per se could be the real underlying mediators. Our current study revealed 25D as a good causal candidate. Ultimately, however, placebo controlled studies should demonstrate that vitamin D3 is an immune modulator in vivo. Regarding these upcoming trials, it is also of interest that we included patients treated with immune modulating drugs. Interestingly, therapy with 1,252D showed synergistic effects with IFN-b in an EAE model of MS. Upcoming clinical trials will most likely assess add-on effects of vitamin D3 on current immune modulating drugs. Results from the present study suggest that it is worthwhile to combine immune-modulating drugs like IFN-b with vitamin D3 in order to further modulate the immune system in a for MS beneficial way. The LMNA gene is alternatively spliced to produce the two intermediate filament proteins termed WY 14643 msds nuclear lamin A/C, which locate to the nuclear lamina, a fibrous structure underlying the inner nuclear membrane. Lamin A/C, emerin and complex which links the nucleoskeleton and cytoskeleton form a variety of macro-protein complexes at the nuclear envelope and together cross-link the nuclear skeleton to the cytoskeleton. These protein complexes function to maintain nuclear architecture and stability and cellular tensegrity. The lamins play important roles in DNA replication, chromatin organization, regulation of gene expression, spatial organization of the nuclear pore and the correct anchorage of the nuclear envelope proteins, cell development, differentiation and apoptosis. The mutations in the LMNA gene has been shown to cause at least nine different autosomal recessive and dominant genetic diseases, collectively called laminopathies. More than 40 mutations in the LMNA gene have been shown to be involved in the severity of the cardiac symptoms, characterized by conduction defect, arrhythmias, left ventricular dysfunction, dilation with heart failure or sudden death. Lamin A/C plays a crucial role in many cellular activities, but it is poorly understood why and how different mutants cause such diverse phenotypes in specific tissues, but other tissues are apparently unaffected, and the identification of the precise molecular mechanisms of LMNA mutations leading to laminopathies is also critical for developing new therapeutic strategies to prevent cardiac dysfunction and sudden death. A novel mutation E82K in lamin A/C gene has been found to cause dilated cardiomyopathy in a large Chinese pedigree with 50 family members. In the current paper, a heart tissue specific transgenic mice expressing LMNA E82K was generated.