Abstract: An example operation may include one or more of receiving a software update at a transport of a subset of transports, validating the software update based on one or more of: a period of time when the software update is in use, and a number of utilizations of the software update by the subset of the transports, propagating the software update based on the validating, to a further subset of transports, wherein the further subset of the transports is larger than the subset of the transports.

Abstract: The disclosure describes a humanized antibody that can bind an extracellular part of human CD89 (human Fc?RI) on human CD89 expressing cells that prevents binding of human IgA to human CD89 when the antibody is bound to said cells. The disclosure also describes the use of such antibodies in combating certain diseases.

Abstract: The invention discloses an antibody that binds an extracellular part of human HVEM on human HVEM-expressing cells, that prevents binding of BTLA to HVEM when the antibody is bound to said extracellular part of HVEM, wherein said antibody displaces BTLA bound to said extracellular part of HVEM. The invention also discloses the use of such an antibody in combating certain diseases.

Abstract: The invention discloses an antibody that can bind an extra-cellular part of human CD89 (human Fc?RI) on human CD89 expressing cells that prevents binding of human IgA to human CD89 when the antibody is bound to said cells and that induces less cell death in said human CD89 expressing cells when compared to the antibody MIP8a. The invention also disclosed the use of such antibodies in combating certain diseases.

Abstract: The invention relates to means and methods that relate to binding molecules that bind human complement factor C2. Specific binding molecules are described with specific C2 activity inhibiting properties. Such binding molecules are useful in the treatment of symptoms of various human diseases among which there is inflammatory disease, neuro-inflammatory disease or ischemia-reperfusion (I/R) injury disease.

Abstract: The invention provide a method for reducing the amount of acidic species and/or increasing the amount of basic species in a composition comprising a recombinant protein or for increasing the specific production rate of mammalian cells expressing a recombinant protein to simplify subsequent clarification and purification of the recombinant protein, said method comprising culturing mammalian cells expressing said recombinant protein in a cell culture medium comprising citrulline.

Abstract: The invention provides antibodies that specifically bind to human CD134. Anti-human CD134 antibodies specifically bind to the extracellular domain of human CD134, including non-OX40 ligand (OX40L) binding domains on human CD134, which is expressed on e.g. activated human conventional effector CD4 and/or CD8 T lymphocytes (Teffs) and on activated human suppressive regulatory CD4 T lymphocytes (Tregs). Humanized anti-human CD134 antibodies are useful (e.g. to empower Teffs anti-cancer effector function and/or to inhibit Tregs suppressive function) for cancer treatment.

Abstract: The invention provides antibodies that specifically bind to human CD134. Anti-human CD134 antibodies specifically bind to the extracellular domain of human CD134, including non-OX40 ligand (OX40L) binding domains on human CD134, which is expressed on e.g. activated human conventional effector CD4 and/or CD8 T lymphocytes (Teffs) and on activated human suppressive regulatory CD4 T lymphocytes (Tregs). Humanized anti-human CD134 antibodies are useful (e.g. to empower Teffs anti-cancer effector function and/or to inhibit Tregs suppressive function) for cancer treatment.

Abstract: The invention relates to means and methods that relate to binding molecules that bind human complement factor C2. Specific binding molecules are described with specific C2 activity inhibiting properties. Such binding molecules are useful in the treatment of symptoms of various human diseases among which there is inflammatory disease, neuro-inflammatory disease or ischemia-reperfusion (I/R) injury disease.

Abstract: The invention provides antibodies that specifically bind to human CD134. Invention anti human CD134 antibodies specifically bind to the extracellular domain of human CD134, including non-OX40 ligand (OX40L) binding domains on human CD134, which is expressed on e.g. activated human conventional effector CD4 and/or CD8 T lymphocytes (Teffs) and on activated human suppressive regulatory CD4 T lymphocytes (Tregs). Invention anti-human CD134 antibodies are useful (e.g. to empower Teffs anti-cancer effector function and/or to inhibit Tregs suppressive function) for cancer treatment.

Abstract: The invention relates to means and methods that relate to binding molecules that bind human complement factor C2. Specific binding molecules are described with specific C2 activity inhibiting properties. Such binding molecules are useful in the treatment of symptoms of various human diseases among which there is inflammatory disease, neuro-inflammatory disease or ischemia-reperfusion (I/R) injury. Disease.

Abstract: The invention provides antibodies that specifically bind to human CD134. Anti-human CD134 antibodies specifically bind to the extracellular domain of human CD134, including non-OX40 ligand (OX40L) binding domains on human CD134, which is expressed on e.g. activated human conventional effector CD4 and/or CD8 T lymphocytes (Teffs) and on activated human suppressive regulatory CD4 T lymphocytes (Tregs). Humanized anti-human CD134 antibodies are useful (e.g. to empower Teffs anti-cancer effector function and/or to inhibit Tregs suppressive function) for cancer treatment.

Abstract: The invention provides antibodies that specifically bind to human CD134. Anti-human CD134 antibodies specifically bind to the extracellular domain of human CD134, including non-OX40 ligand (OX40L) binding domains on human CD134, which is expressed on e.g. activated human conventional effector CD4 and/or CD8 T lymphocytes (Teffs) and on activated human suppressive regulatory CD4 T lymphocytes (Tregs). Humanized anti-human CD134 antibodies are useful (e.g. to empower Teffs anti-cancer effector function and/or to inhibit Tregs suppressive function) for cancer treatment.

Abstract: The invention provides antibodies that specifically bind to human CD134. Invention anti-human CD134 antibodies specifically bind to the extracellular domain of human CD134, including non-OX40 ligand (OX40L) binding domains on human CD134, which is expressed on e.g. activated human conventional effector CD4 and/or CD8 T lymphocytes (Teffs) and on activated human suppressive regulatory CD4 lymphocytes (Tregs). Invention anti-human CD134 antibodies are useful (e.g. to empower Teffs anti-cancer effector function and/or to inhibit Tregs suppressive function) for cancer treatment.

Abstract: The invention provides antibodies that specifically bind to human CD134. Invention anti-human CD134 antibodies specifically bind to the extracellular domain of human CD134, including non-OX40 ligand (OX40L) binding domains on human CD134, which is expressed on e.g. activated human conventional effector CD4 and/or CD8 T lymphocytes (Teffs) and on activated human suppressive regulatory CD4 T lymphocytes (Tregs). Invention anti-human CD134 antibodies are useful (e.g. to empower Teffs anti-cancer effector function and/or to inhibit Tregs suppressive function) for cancer treatment.

Abstract: The invention relates to means and methods that relate to binding molecules that bind human complement factor C2. Specific binding molecules are described with specific C2 activity inhibiting properties. Such binding molecules are useful in the treatment of symptoms of various human diseases among which there is inflammatory disease, neuro-inflammatory disease or ischemia-reperfusion (I/R) injury. Disease.

Abstract: The invention provides antibodies that specifically bind to human CD134. Invention anti-human CD134 antibodies specifically bind to the extracellular domain of human CD134, including non-OX40 ligand (OX40L) binding domains on human CD134, which is expressed on e.g. activated human conventional effector CD4 and/or CD8 T lymphocytes (Teffs) and on activated human suppressive regulatory CD4 T lymphocytes (Tregs). Invention anti-human CD134 antibodies are useful (e.g. to empower Teffs anti-cancer effector function and/or to inhibit Tregs suppressive function) for cancer treatment.

Abstract: The invention provides antibodies that specifically bind to human CD134. Anti-human CD134 antibodies specifically bind to the extracellular domain of human CD134, including non-OX40 ligand (OX40L) binding domains on human CD134, which is expressed on e.g. activated human conventional effector CD4 and/or CD8 T lymphocytes (Teffs) and on activated human suppressive regulatory CD4 T lymphocytes (Tregs). Humanized anti-human CD134 antibodies are useful (e.g. to empower Teffs anti-cancer effector function and/or to inhibit Tregs suppressive function) for cancer treatment.

Abstract: Methods for inducing tolerance to a transplant in a subject are disclosed. The methods comprise administering multiple doses of a therapeutically effective amount of a CD40 antagonist alone or in combination with a CD86 antagonist, wherein the first dose of the antagonist is given before or at the time of transplantation; and administering multiple doses of a therapeutically effective amount of an immunosuppressive drug, wherein the first dose of the immunosuppressive drug is given at least several days after transplantation.

Abstract: The invention relates to the field of immunology, gene therapy, and medicine. More specifically, the invention relates to the identification of a molecule capable of interacting with a soluble and/or cell-bound form of CD163 and, as a result of the interaction, an immune response is either instigated or suppressed in an organism. Furthermore, it relates to the preparation of a pharmaceutical composition including the molecule and/or antagonist I and/or agonist I thereof, and/or an isolated CD163 and/or an antagonist II or agonist II thereof, for the therapeutic or prophylactic treatment of an individual with an immune response disorder, e.g., inflammation, cancer, or infection.