The invention is concerned with a fusion protein comprising interleukin 13 and a regulatory cytokine, for example, an interleukin chosen from interleukin 4, interleukin 10, interleukin 27, interleukin 33, transforming growth factor beta 1, transforming growth factor beta 2, and interleukin 13, a nucleic acid molecule encoding such fusion protein, a vector comprising such nucleic acid molecule, and a host cell comprising such nucleic acid molecule or such vector. The invention further pertains to a method for producing such fusion protein. The fusion protein or a gene therapy vector encoding the fusion protein may be used in the prevention or treatment of a condition characterized by pathological pain, chronic pain, neuro-inflammation and/or or neurodegeneration.

The present invention relates to: a recombinant peptide in which a Mitochondria Localization Sequence (MLS) peptide and the Signal Transducer and Activator of Transcription 3 (STAT3) are fused to each other; a recombinant vector carrying a polynucleotide coding for the recombinant peptide; and a composition comprising the recombinant peptide or the recombinant vector as an active ingredient for prevention or treatment of autoimmune disease or inflammatory disease, wherein the recombinant peptide or the recombinant vector allows STAT3 to be overexpressed in the mitochondria to enhance the mitochondrial function, resulting in inhibiting the expression of inflammatory cytokines including IL-17, whereby the composition may be advantageously used for preventing or treating autoimmune disease or inflammatory diseases.

The present invention relates to a composition for treating neuroinflammatory disease comprising a complement component 8 gamma protein or a fragment thereof, and more particularly, to use for treating neuroinflammatory disease of a complement component 8 gamma protein or a fragment thereof which exhibits an effect of reducing the expression of inflammatory cytokines in microglia. The composition of the present invention has effects of reducing Alzheimer's abnormal behavior patterns and reducing the secretion of neuroinflammatory cytokines in brain microglia and thus can be very usefully used for development of an agent for preventing or treating neuroinflammatory disease.

The disclosure relates, in some aspects, to compositions and methods for treatment of central nervous system (CNS) diseases, for example Parkinson's disease (PD) and Gaucher disease. In some embodiments, the disclosure provides expression constructs comprising a transgene encoding one or more CNS disease-associated gene products and/or one or more an inhibitory nucleic acids targeting a CNS disease-associated gene or gene product. In some embodiments, the disclosure provides methods of treating CNS diseases by administering such expression constructs to a subject in need thereof.

The present invention relates to a compound comprising (1) a first binding moiety that binds to an Interleukin 4 receptor; and (2) a second binding moiety that binds to a cytokine receptor (e.g., an Interleukin 10 receptor, Interleukin 13 receptor, interleukin 27 receptor, interleukin 33 receptor, or transforming growth factor beta 1/2 receptor). Compounds of the disclosure cluster or crosslink the IL4 receptor and a cytokine receptor, and surprisingly, elicit unique responses in the nervous system, including unique signaling and gene expression profiles. The signaling and gene expression profiles generated IL4-cytokine fusion proteins of the disclosure are distinct from those observed in response to the combination of IL4 and the cytokine, and contribute to the superior therapeutic effects over the combination of the component parts.

The current invention describes a laboratory animal model for dirofilarial nematodes wherein said laboratory animal is fed a dietary admixture of laboratory feed containing an immunosuppressing agent, for example, a glucocorticoid. The invention also describes the use of the laboratory animal model for screening endoparasiticides for the treatment and/or prevention of filarial nematode infections in animals.

The present disclosure relates to a method for establishing an oral ulcer animal model with Yin-deficiency and fire-excess syndrome based on sleep deprivation, comprising the following steps of: burning buccal mucosa of a rat with phenol to cause a white injury, and obtaining the oral ulcer animal model after 24-48 h; placing the animal model in a sleep deprivation device for 2-7 days; wherein the device is composed of a mouse box in which a plurality of platforms with a diameter of 4-8 cm are arranged at an interval of 10-20 cm from each other; and water is filled among the platforms, and the platforms are about 0.1-2 cm higher than a water surface. The present disclosure overcomes the defects of single evaluation index, short model duration, and unconformity of etiology and clinic existed in the prior art.

A method of treating at least one of septicemia, endotoxemia or a bacterial infection in a subject can include administering to the subject a composition containing a therapeutically effective amount of a haloperoxidase. The haloperoxidase can be myeloperoxidase or eosinophil peroxidase. The haloperoxidase can inhibit lipopolysaccharide or Lipid A activity in the subject; as a non-limiting example, the haloperoxidase is not engaged in active haloperoxidase activity, but available for LPS or Lipid A binding and inhibition.

The present disclosure relates to a method for preparing an Alzheimer's disease (AD) animal model, including: selecting healthy male human ApoE4 transgenic mice, and intraperitoneally injecting a 4 mmol/L Al(mal).sub.3 solution at a volume of 10 ml/kg, with aluminum exposure for 60 days, and interval time of 2 days for every 5 days, to obtain an AD animal model co-induced by genetic and environmental factors which are interacted without being simply superimposed. The AD animal model established according to the method of the examples in the present disclosure can express the characteristic pathological changes of AD and has the characteristics of learning and memory impairment. The AD animal model provided by the present disclosure can be used for drug screening and AD mechanism research, and has the advantages of stable properties, prominent reproducibility, easy operation, and low cost.

Disclosed herein are conditioning regimens and methods for inducing MHC- or HLA-mismatched mixed chimerism by conditioning a recipient with radiation-free, low-doses of cyclophosphamide (CY), pentostatin (PT), and anti-thymocyte globulin (ATG) prior to transplantation of donor bone marrow cells. In certain embodiments, the donor bone marrow cells may be CD4+ T-depleted bone marrow cells. The conditioning regimens and methods may also include administering one or more populations of conditioning donor cells selected from donor CD4.sup.+ T-depleted spleen cells, donor CD8.sup.+ T cells, and donor G-CSF-mobilized peripheral blood mononuclear cells. The conditioning regimen is clinically acceptable and can be used for treating hereditary hematological diseases and autoimmune diseases, as well as for promoting organ transplantation immune tolerance.