It was found that bacteria belonging to the genus Clostridium induce accumulation of regulatory T cells (Treg cells) in the colon. Moreover, the present inventors found that regulatory T cells (Treg cells) induced by from these bacteria suppressed proliferation of effector T-cells. From these findings, the present inventors found that the use of bacteria belonging to the genus Clostridium or a physiologically active substance derived therefrom made it possible to induce proliferation or accumulation of regulatory T cells (Treg cells), and further to suppress immune functions.

It was found that bacteria belonging to the genus Clostridium induce accumulation of regulatory T cells (Treg cells) in the colon. Moreover, the present inventors found that regulatory T cells (Treg cells) induced by from these bacteria suppressed proliferation of effector T-cells. From these findings, the present inventors found that the use of bacteria belonging to the genus Clostridium or a physiologically active substance derived therefrom made it possible to induce proliferation or accumulation of regulatory T cells (Treg cells), and further to suppress immune functions.

Provided are a psoriasis-induced transgenic animal model overexpressing the Pellino homolog 1 (Peli1) gene according to doxycycline administration, and a use thereof. The transgenic animal model of the present disclosure exhibited similarity to phenotypes shown in patients with psoriasis, due to overexpression of the Pellino homolog 1 (Peli1) gene according to doxycycline administration. It is anticipated that the transgenic animal model may be usefully used in clinical studies, such as screening for a candidate drug for the treatment of psoriasis. Additionally, it is anticipated that a peptide derived from the Peli1 FHA domain targeting the FHA binding motif that inhibits normal substrate binding between a substrate protein and the Peli1 protein may be usefully used in the development of new drugs for psoriasis-associated diseases. Moreover, by confirming an expression level of the Peli1 protein, it is anticipated to be usefully used in evaluating the severity of patients with psoriasis.

The invention relates to novel therapeutic approaches to cancer treatment that exploits tumor suppressor functions of DKK3b by site-specific delivery of DKK3b. Novel therapeutics and methods for treating tumors and cancers utilizing DKK3b tumor suppressor functions are disclosed.

Pericytes are mural cells of brain capillaries that degenerate in multiple neurological disorders. Pericytes regulate neurovascular functions, but their role in the adult brain and disease is still poorly understood because of the lack of adequate pericyte-specific experimental models. All current pericyte-deficient models are not pericyte specific, and carry an inherited embryonic trait. Here, the Inventors generated an inducible pericyte-specific Cre line using a double-promoter strategy. The Inventors ablated adult mouse pericytes expressing Cre-dependent diphtheria toxin receptor after toxin administration. Pericyte ablation led to a rapid dysregulation of cerebral blood flow and blood-brain barrier breakdown. This was followed by behavioral deficits and neurodegenerative changes. These findings show that circulatory deficits leading to secondary neurodegeneration develop immediately after pericyte loss.

Disclosed herein are genomically edited livestock animals and in particular, swine for use as models of polycystic kidney disease (PKD) especially ARPKD and ADPKD. The animals disclosed herein are heterozygous, homozygous or compound heterozygous for mutations of the PKD1 and/or PKD2 genes and/or the PKHD1 gene. The mutations expressed in these models include mutations identified in humans responsible for PKD. In some embodiments, the expression is inducible. In further embodiments, the edit is introduced by an all in one expression cassette following the birth of the animal. Induction of the cassette allows for study of the model throughout the time course of the disease.

The present invention relates to expression cassettes and vectors comprising Alzheimer's disease-related genes and a cell line transformed by the disclosed expression cassettes and vectors, and more specifically, the expression cassettes according to the present invention comprise amyloid precursor protein (APP), Tau protein, and presenilin-1 (PS1) genes associated with Alzheimer's disease so that mutant genes thereof can be simultaneously expressed. Additionally, the present invention relates to a cell line transformed by the disclosed expression cassettes or vectors comprising APP, Tau protein, and PS1 genes, and further, to an animal model transformed by the vectors or cell line.

Methods are disclosed herein for treating a subject with type 2 diabetes. These methods include administering to the subject a therapeutically effective amount of an inhibitor that decreases expression of smad2. In some embodiments, the inhibitor is an inhibitory RNA, a small molecule, or a CRISPR-Cas9 system.

The invention is directed to compositions and methods for treating or reducing the likelihood of the development of epilepsy in an individual. The method comprises administering to the central nervous system of an individual in need of such treatment a therapeutically effective amount of an agent capable of increasing the expression and/or activity of miR-128.

The present disclosure includes compositions and methods for treating gastrointestinal inflammatory disease and/or cancers. In certain aspects, the disclosure includes an isolated cell comprising a nucleic acid vector comprising a gene encoding the transcription factor ZBTB20 which is operably linked to a promoter.