A method and system for the treatment of honey bees (Apis mellifera), bats, and butterflies protects them from various life threatening conditions, including Colony Collapse Disorder and in particular, provides honey bees with the ability to assimilate and degrade pesticides such as neonicotinoids and fipronil.

In one aspect, a method of treating a subject having or at risk of having graft-versus-host disease (GvHD) generally includes administering to the subject a plurality of myeloid-derived suppressor cells (MDSCs) effective to ameliorate at least one symptom or clinical sign of graft-versus-host disease compared to a suitable control subject. In another aspect, a method of treating a tumor in a subject generally includes administering to the subject an anti-tumor therapy and co-administering to the subject an inflammasome inciting agent in an amount effective to increase inflammasome activation of MDSCs sufficiently to reduce suppressor function of the MDSCs.

The present invention relates to (isolated) recombinant proteins, also referred to as improved MAT (iMAT) molecules, comprising at least one translocation module, at least one targeting module and at least one antigen module, wherein at least one cysteine residue is substituted with a different amino acid residue. Such iMAT molecules are useful specifically as vaccines, e.g. for therapy and/or prevention of allergies and/or infectious diseases and/or prevention of transmission of infectious diseases in animals, more preferably ruminants, pigs, dogs and/or cats, but excluding equines. The present invention further relates to nucleic acids encoding such iMAT molecules, corresponding vectors and primary cells or cell lines.

The present invention relates to an engineered regulatory T cell (Treg) comprising a T cell receptor (TCR) which is capable of specifically binding to a myelin basic protein (MBP) peptide or variant or fragment thereof when the peptide is presented by a major histocompatibility complex (MHC) molecule. The present invention further relates to methods for providing an engineered Treg and to methods and uses of said engineered Treg and vectors and kits of vectors encoding said Treg.

The present invention relates generally to the field of antigen binding proteins such as antibodies, in particular those which bind to HLA-DQ2.5:DQ2.5-glia-α1a, or which bind to HLA-DQ2.5:DQ2.5-glia-α2. The invention further relates to compositions and immunoconjugates comprising such antibodies and to methods of producing such antibodies. The invention also relates to methods and uses which employ such antibodies, for example in the treatment of celiac disease.

The present invention provides methods for inducing tolerance or suppressing an immune response to an antigen by passing a cell suspension containing an immune cell through a constriction, wherein the constriction deforms the cell thereby causing a perturbation of the cell such that an antigen and/or tolerogenic factor enters the cell, thereby generating a tolerogenic and/or immunosuppressive immune cell. In some embodiments, the tolerogenic and/or immunosuppressive immune cell is delivered to an individual and presentation of the antigen induces tolerance and/or suppresses an immune response to the antigen.

The instant disclosure provides antibodies that specifically bind to CD137 (e.g., human CD137) and increases CD137 function. Also provided are pharmaceutical compositions comprising these antibodies, nucleic acids encoding these antibodies, expression vectors and host cells for making these antibodies, and methods of treating a subject using these antibodies.

The present invention relates to IgE epitope-like peptides which have ability to bind to allergen specific IgE paratopes. Said allergen specific IgEs are bound to effector cells of allergic patients. The IgE epitope-like peptides of the invention cover the paratopes of said IgE bound on effector cells, prevent biding of causative allergen on said IgE on effector cells, and thereby prevent degranulation and secretion of mediators of allergic inflammation from effector cells, after contact with the causative allergen. The present invention relates to the methods of using such IgE epitope-like peptides for therapy of allergic reaction. Said allergic reaction is caused by exposure to the causative allergen.

The present invention is based, in part, on methods for modulating regulatory T cells, regulatory B cells, and immune responses using modulators of the APRIL-TACI interaction.

Disclosed herein, in one aspect, is a method of reducing immunogenicity, comprising administering to a patient receiving or having received a biological therapeutic agent, an effective amount of B cell inhibitor that is non-depletional. Related compositions are also provided.