Determinants of expression variability.

The amount of tissue-specific expression variability (EV) across individuals is an essential characteristic of a gene and believed to have evolved, in part, under functional constraints. However, the determinants and functional implications of EV are only beginning to be investigated. Our analyses based on multiple expression profiles in 41 primary human tissues show that a gene's EV is significantly correlated with a number of features pertaining to the genomic, epigenomic, regulatory, polymorphic, functional, structural and network characteristics of the gene.

Widespread evidence of viral miRNAs targeting host pathways.

Background: MicroRNAs (miRNA) are regulatory genes that target and repress other RNA molecules via sequence-specific binding. Several biological processes are regulated across many organisms by evolutionarily conserved miRNAs. Plants and invertebrates employ their miRNA in defense against viruses by targeting and degrading viral products.

Increased Th17 and regulatory T cell responses in EBV-induced gene 3-deficient mice lead to marginally enhanced development of autoimmune encephalomyelitis.

EBV-induced gene 3 (EBI3)-encoded protein can form heterodimers with IL-27P28 and IL-12P35 to form IL-27 and IL-35. IL-27 and IL-35 may influence autoimmunity by inhibiting Th17 differentiation and facilitating the inhibitory roles of Foxp3(+) regulatory T (Treg) cells, respectively. In this study, we have evaluated the development of experimental autoimmune encephalomyelitis (EAE) in EBI3-deficient mice that lack both IL-27 and IL-35.

IL27: its roles in the induction and inhibition of inflammation.

IL27 is the newest member of the IL6/IL12 family. It consists of Epstein-Barr virus-induced gene 3 (EBI3) and p28 subunits and signals through the IL27 receptor complex formed by WSX-1 and gp130 subunits. IL27-IL27 receptor interaction was initially shown to induce an early signal for the induction of Th1 responses.

Autoreactive T cells escape clonal deletion in the thymus by a CD24-dependent pathway.

Despite negative selection in the thymus, significant numbers of autoreactive T cells still escape to the periphery and cause autoimmune diseases when immune regulation goes awry. It is largely unknown how these T cells escape clonal deletion. In this study, we report that CD24 deficiency caused deletion of autoreactive T cells that normally escape negative selection.

CD24 on the resident cells of the central nervous system enhances experimental autoimmune encephalomyelitis.

CD24 is a cell surface glycoprotein that is expressed on both immune cells and cells of the CNS. We have previously shown that CD24 is required for the induction of experimental autoimmune encephalomyelitis (EAE), an experimental model for the human disease multiple sclerosis (MS). The development of EAE requires CD24 expression on both T cells and non-T host cells in the CNS.