The present invention is directed to use of kifunensine for increasing sialylation of a glycosylated polypeptide, wherein a cell that produces the glycosylated polypeptide is contacted with kifunensine. Also provided are related methods for increasing sialylation of a glycosylated polypeptide and producing a glycosylated polypeptide, as well as glycosylated polypeptides and pharmaceutical compositions comprising the same, and their use in medicine.

This disclosure describes genetically engineered natural killer (NK) cells, pharmaceutical compositions that include these NK cells, and methods of making and using these NK cells.

It is an object of the present invention to provide a method for efficiently producing a B cell population comprising B cells that recognize a specific antigen. According to the present invention, provided is a method for producing a B cell population, comprising: a step (c) of culturing a cell population comprising B cells together with a specific antigen in the absence of IL-21, in the absence of IL-4, and in the presence of a cytokine other than IL-21 and IL-4, while giving stimulation mediated by CD40 and a BAFF receptor to the cells; and a step (d) of culturing the cell population comprising B cells, while giving stimulation mediated by has to the cells, so as to obtain a B cell population comprising B cells that recognize the specific antigen.

The present disclosure provides compositions comprising miR-3132 and one or more pharmaceutical agents that upregulate TNF-related apoptosis-inducing ligand (TRAIL) or activate TRAIL signaling pathway, and methods for treating a cancer comprising administering miR-3132, or a composition comprising miR-3132 and one or more pharmaceutical agents that upregulate TRAIL or activate TRAIL signaling pathway, to a subject.

Disclosed are agents for treating or preventing cancers. More particularly, the present invention discloses therapeutic combinations comprising antagonists of receptor of NF-κB (RANK) ligand and immune checkpoint molecules in methods and compositions for treating or inhibiting the development, progression or recurrence of cancers, including metastatic cancers.

The present invention provides Tenascin-3 FnIII domain-based scaffolds that specifically bind to CD40L. The invention further provides engineered variants with increased affinity for the target. The present invention is also related to engineered scaffolds as prophylactic, diagnostic, or therapeutic agents, in particular for therapeutic uses against SLE and other autoimmune diseases and conditions.

This invention provides, and in certain specific but non-limiting aspects relates to: assays that can be used to predict whether a given ISV will be subject to protein interference as described herein and/or give rise to an (aspecific) signal in such an assay (such as for example in an ADA immunoassay). Such predictive assays could for example be used to test whether a given ISV could have a tendency to give rise to such protein interference and/or such a signal; to select ISV's that are not or less prone to such protein interference or to giving such a signal; as an assay or test that can be used to test whether certain modification(s) to an ISV will (fully or partially) reduce its tendency to give rise to such interference or such a signal; and/or as an assay or test that can be used to guide modification or improvement of an ISV so as to reduce its tendency to give rise to such protein interference or signal; —methods for modifying and/or improving ISV's to as to remove or reduce their tendency to give rise to such protein interference or such a signal; —modifications that can be introduced into an ISV that remove or reduce its tendency to give rise to such protein interference or such a signal; ISV's that have been specifically selected (for example, using the assay(s) described herein) to have no or low(er)/reduced tendency to give rise to such protein interference or such a signal; modified and/or improved ISV's that have no or a low(er)/reduced tendency to give rise to such protein interference or such a signal.

Improved anti-CD154 antibodies are provided herein which have ablated FcR binding and/or complement binding/activation. The use of these antibodies for inducing tolerance and treating immune diseases including autoimmunity, inflammation and allergic disorders is disclosed herein.

The present disclosure relates to methods of detecting free (active) LIGHT in biological samples to diagnose conditions associated with elevated free LIGHT, as well as to predict the effectiveness of anti-LIGHT therapies. The disclosure also relates to treating such conditions with anti-LIGHT antibodies. Conditions include acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), optionally wherein the ALI and ARDS are associated with viral infection, including coronavirus infection. Conditions also include Crohn's Disease or an inflammatory condition associated with Crohn's Disease.

VH domain, in which: (i) the amino acid residue at position 112 is one of K or Q; and/or (ii) the amino acid residue at position 89 is T; and/or (iii) the amino acid residue at position 89 is L and the amino acid residue at position 110 is one of K or Q; and (iv) in each of cases (i) to (iii), the amino acid at position 11 is preferably V; and in which said VH domain contains a C-terminal extension (X)n, in which n is 1 to 10, preferably 1 to 5, such as 1, 2, 3, 4 or 5 (and preferably 1 or 2, such as 1); and each X is an (preferably naturally occurring) amino acid residue that is independently chosen, and preferably independently chosen from the group consisting of alanine (A), glycine (G), valine (V), leucine (L) or isoleucine (I).