The present invention pertains to a non-human genetically modified animal with increased susceptibility to infection with a human virus. The invention suggests to genetically impair the expression of newly identified viral infection repression factors CD302, Cr11, Ndufc2, AW112010, Scarb2 and Zc3hav1, which markedly improves infection with human viruses in none-human hosts. Furthermore provided are methods for the generation of the animal of the invention, methods for increasing or reducing the susceptibility of a cell to viral infection, methods for screening novel modulators of viral infection as well as new therapy options for the treatment of viral diseases, in particular hepatitis C.

The present invention provides a protein construct comprising: a) at least two monomers each of which comprises a C-type lectin domain of CD23, wherein each monomer can bind to IgE; and b) an entity which can bind to the neonatal Fc receptor (FcRn); wherein said protein construct comprises a linker, and wherein said linker is used to link said monomer comprising a C-type lectin domain of CD23 to said entity which can bind to FcRn. Therapeutic uses of the constructs, for example in anti-IgE therapy or for use in the treatment or prevention of an IgE related disease or condition are also provided.

The present invention provides a tumor immunotherapy target and use thereof, specifically provides use of the LSECtin expressed by infiltrating tumor-associated macrophage and BTN3A3 expressed by tumor solely or in combination as a target in tumor immunotherapy, and further provides a substance capable of inhibiting the activity of LSECtin expressed by infiltrating tumor-associated macrophage, the activity of BTN3A3 expressed by tumor, or the interaction of the LSECtin with BTN3A3, including RNA molecules, fusion protein BTN3A3-Ig, and monoclonal antibody 5E08, which can be used as an active ingredient to prepare a tumor immunotherapy drug, and is suitable for industrial applications.

The present disclosure provides treatments for neurodegenerative disorders and more particularly to methods for treatment of patients with Multiple Sclerosis (MS), Amyotrophic Lateral Sclerosis (ALS), or Alzheimer's disease of different degrees of severity. The methods for treatment of patients who have suffered neurodegenerative diseases and specifically MS, ALS, or Alzheimer's disease includes administering a xenon gas mixture in subjects with elevated levels of neurodegenerative microglia (MGnD), e.g., determined based on levels of inflammatory biomarkers, measured in blood, serum and CSF, or levels of CLEC7A (Dectin-1)/Translocator Protein (TSPO) expression, e.g., measured using TSPO imaging.

The present invention relates to a method of generating γδ T cells having at least one down-regulated co-inhibitory receptor, the method comprising the steps of: (a) culturing a population of cells comprising γδ T cells with a phosphoantigen to expand the γδ T cells; and (b) culturing the expanded γδ T cells with artificial antigen-presenting cells expressing a Fc receptor, and an anti-CD3 antibody. The present invention also relates to γδ T cells generated according to a method of the present invention, as well as methods of treatment and medical uses thereof.

The present invention relates to a novel method for the affinity purification of proteins of interest in a single step, based on the lectin activity of the CRD (Carbohydrate Recognition Domain) of a galectin or part of said domain retaining the ability to bind β-galactosidase derivative.

The disclosure features lipid nanoparticle (LNP) compositions comprising immune checkpoint inhibitor molecules and uses thereof. The LNP compositions of the present disclosure comprise mRNA therapeutics encoding immune checkpoint inhibitor polypeptides, e.g., PD-L1, PD-L2, B7-H3, B7-H4, CD200 Galectin 9 and CTLA4. The LNP compositions of the present disclosure can reprogram dendritic cells, suppress T cells and/or induce immune tolerance in vivo.

Provided are modified therapeutic cells comprising a first heterologous nucleic acid sequence encoding a simian ICP47 (sICP47) protein or a functional variant thereof. In some embodiments, the modified therapeutic cell further comprises a second heterologous nucleic acid sequence encoding an agonist of a natural killer cell inhibitory receptor. Also provided are methods of treatment using the modified therapeutic cells.

Engineered trimeric CD70 proteins for use in ex vivo T cell manufacturing are described. Use of the proteins during manufacturing creates expanded T cell populations with enhanced properties such as earlier proliferation in culture; selective expansion of nave and memory T cell subsets; longer persistence in vivo following administration to a subject; and improved therapeutic effect. Use of the proteins as therapeutics provide anti-cancer and anti-viral effects. The proteins can also be used as agonistic cell culture reagents in in vitro uses.

The present disclosure relates to genetically modified non-human animals that express a human or chimeric (e.g., humanized) CD94 and/or NKG2A, and methods of use thereof.