The invention relates to using cell free nucleosome levels to identify patients at risk of developing a NETosis associated adverse reaction to the infection. The methods are used to monitor the progress of a disease and assigning a risk of an adverse outcome in a patient suffering from an infection.

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.

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.

The present invention relates to a novel compound represented by Formula 1, functioning as a sphingosine-1-phosphate receptor agonist useful for treating autoimmune disorders, a preparation method therefor, a pharmaceutical composition containing the same as an active ingredient, and a use. The compound according to the present invention has an effect in extensive autoimmune diseases and chronic inflammatory diseases, including relapsing-remitting multiple sclerosis, and can also be used for treating or preventing immunoregulatory disorders.

The present invention relates to a novel compound represented by Formula 1, functioning as a sphingosine-1-phosphate receptor agonist useful for treating autoimmune disorders, a preparation method therefor, a pharmaceutical composition containing the same as an active ingredient, and a use. The compound according to the present invention has an effect in extensive autoimmune diseases and chronic inflammatory diseases, including relapsing-remitting multiple sclerosis, and can also be used for treating or preventing immunoregulatory disorders.

Methods of expanding T cells ex vivo comprising contacting the T cells with antibody molecules that bind to TCR Vβ regions are described. T cells comprise one or more nucleic acid molecule encoding an exogenous cellular receptor, for example, a chimeric antigen receptor (CAR) or an exogenous T cell receptor (TCR).

Methods of expanding T cells ex vivo comprising contacting the T cells with antibody molecules that bind to TCR Vβ regions are described. T cells comprise one or more nucleic acid molecule encoding an exogenous cellular receptor, for example, a chimeric antigen receptor (CAR) or an exogenous T cell receptor (TCR).

The present disclosure relates to compounds which modulate the activity of Toll-like receptor (TLR) proteins, including agonists or activators, partial agonists, and antagonists. Of particular interest of compounds that modulate the activity of TLR2, as well as methods of using such compounds to treat cancer and other disorders associated with a TLR2 pathway.

The present invention relates to methods for developing engineered T-cells for immunotherapy that are non-alloreactive. The present invention relates to methods for modifying T-cells by inactivating both genes encoding T-cell receptor and an immune checkpoint gene to unleash the potential of the immune response. This method involves the use of specific rare cutting endonucleases, in particular TALE-nucleases (TAL effector endonuclease) and polynucleotides encoding such polypeptides, to precisely target a selection of key genes in T-cells, which are available from donors or from culture of primary cells. The invention opens the way to standard and affordable adoptive immunotherapy strategies for treating cancer and viral infections.

Provided are cells containing exogenous antigen and uses thereof.