Abstract: Disclosed herein are methods of using anti-ILT5 antibodies and ILT5-binding fragments thereof to induce an immunostimulatory effect in a T cell when such a T cell is contacted with an antigen presenting cell (APC) that has been previously contacted with the anti-ILT5 antibody or ILT5-binding fragment. Also disclosed herein are methods of using anti-ILT5 antibodies and ILT5-binding fragments thereof to inhibit a response in a T cell (e.g., a pro-liferative response) when such a T cell is concomitantly contacted, or has previously been contacted, with an APC, which APC is simultaneously contacted with the anti-ILT5 antibody or ILT5-binding fragment. Also disclosed herein are methods of using anti-ILT5 antibodies and ILT5-binding fragments thereof for the treatment of various diseases and for use as immunostimulatory adjuvants.

Abstract: Disclosed herein are antibodies and ILT5-binding fragments thereof that specifically bind to ILT5, e.g., human ILT5 (hILT5), and pharmaceutical compositions comprising such ILT5-binding antibodies and ILT5-binding fragments thereof.

Abstract: Inducing tolerance in a primate by use of a compound, or a combination of at least two compounds, that has certain characteristics when tested in vitro. The compound, alone or in combination, is preferably TRX1 antibody and the compound or combination is preferably used in accordance with a specified dosing regimen.

Abstract: The present invention provides binding molecules that specifically bind to ILT3, e.g., human ILT3 (hILT3), on antigen presenting cells, such as for example, monocytes, macrophages and dendritic cells (DC), e.g., monocyte-derived dendritic cells (MDDC). The binding molecules of the invention are characterized by binding to hILT3 with high affinity and downmodulating immune responses in vitro, e.g., downmodulating alloimmune responses; the production of inflammatory cytokines by dendritic cells, e.g., monocyte-derived dendritic cells (MDDC); the upregulation of costimulatory molecules by DC, e.g., MDDC; and/or calcium flux in monocytes. In addition, the binding molecules upregulate the expression of inhibitory receptors on dendritic cells, e.g., immature dendritic cells. Surprisingly, these same binding molecules which downmodulate immune responses in vitro, are immunostimulatory in vivo. Various aspects of the invention relate to binding molecules, and pharmaceutical compositions thereof.

Abstract: The present invention provides binding molecules that specifically bind to ILT3, e.g., human ILT3 (hILT3), on antigen presenting cells, such as for example, monocytes, macrophages and dendritic cells (DC), e.g., monocyte-derived dendritic cells (MDDC). The binding molecules of the invention are characterized by binding to hILT3 with high affinity and downmodulating immune responses in vitro, e.g., downmodulating alloimmune responses; the production of inflammatory cytokines by dendritic cells, e.g., monocyte-derived dendritic cells (MDDC); the upregulation of costimulatory molecules by DC, e.g., MDDC; and/or calcium flux in monocytes. In addition, the binding molecules upregulate the expression of inhibitory receptors on dendritic cells, e.g., immature dendritic cells. Surprisingly, these same binding molecules which downmodulate immune responses in vitro, are immunostimulatory in vivo. Various aspects of the invention relate to binding molecules, and pharmaceutical compositions thereof.

Abstract: The present invention features methods for reducing protein A contamination in a binding molecule preparation, e.g., a therapeutic binding molecule preparation, comprising residual protein A, or fragments thereof.

Abstract: The present invention is based, at least in part, on the finding that certain molecules are preferentially associated with effector T cells or regulatory T cells. Accordingly, immune responses by one or the other subset of cells can be preferentially modulated. The invention pertains, e.g., to methods of modulating (e.g., up- or down-modulating), the balance between the activation of regulatory T cells and effector T cells leading to modulation of immune responses and to compositions useful in modulating those responses. The invention also pertains to methods useful in diagnosing, treating, or preventing conditions that would benefit from modulating effector T cell function relative to regulatory T cell function or from modulating regulatory T cell function relative to effector T cell function in a subject.

Abstract: The present invention provides combination therapies that employ a GITR binding molecule in combination with one or more additional agents.

Abstract: The present invention is based, at least in part, on the finding that tolerance can be induced by inhibition of CD4+ cells (and optionally CD8+ cells). Accordingly, the optimized dosing methods of the invention are useful in treating a primate, e.g., a human, by inhibiting CD4+ T cells to induce tolerance to at least one antigen, e.g., self or foreign, such as for inducting tolerance in a primate against a soluble or a cell bound antigen (e.g., an allogeneic or xenogeneic transplanted antigen).