Abstract: Compositions and methods for treating diseases associated with expression of cluster differentiation 33 (CD33) and/or cluster differentiation 5 (CD5) involve two chimeric antigen receptors (CARs) specific to CD33 and CD5 and T cells with CD33 and CD5 dual-CAR. Methods of administering a genetically modified T cell expressing the dual-CAR can be used for autologous and allogeneic treatment of T cell malignancies.

Abstract: Several embodiments of the methods and compositions disclosed herein relate to immune cells that are engineered to express chimeric antigen receptors and/or genetically modified to enhance one or more aspects of the efficacy of the immune cells in cellular immunotherapy. Several embodiments relate to genetic modifications which reduce potential side effects of cellular immunotherapy. In several embodiments, combinations of cells are used to achieve both rapid and long-term tumor reduction with reduced or eliminated potential for graft versus host effects.

Abstract: Several embodiments disclosed herein relate to methods and processes for the co-expansion of multiple types of immune cells, in order to generate a mixed cell population. Some embodiments relate to the use of various stimuli specific to the various subpopulations to achieve expansion of those subpopulations at a particular time in a culturing process in order to generate an expanded population of immune cells having a desired ratio of the various subpopulations. In several embodiments, such mixed cell populations exhibit desirable characteristics, such as cytotoxic effects against tumor cells that enhance the efficacy of cancer immunotherapy.

Abstract: Embodiments of the disclosure encompass methods and compositions related to cancer treatment with particular immune effector cells as adoptive immunotherapy and/or with soluble proteins to which the immune effector cells are able to bind. In some cases, the soluble proteins are molecular adaptors that allow targeting of cancer cells that lack expression of a tumor antigen to which the adoptive immunotherapy is directed. In some embodiments, the soluble proteins are exogenously provided as cytokine-cytokine receptor pairs that improve adoptive immunotherapy.

Abstract: The present invention regards methods and/or compositions related to Natural Killer T cells that are engineered to harbor an expression construct that encodes IL-2, IL-4, IL-7, and/or IL-15 and additionally or alternatively comprise a chimeric antigen receptor (CAR). In specific embodiments, the CAR is a CAR that targets the GD2 antigen, for example in neuroblastoma.

Abstract: The present invention regards methods and/or compositions related to Natural Killer T cells that are engineered to harbor an expression construct that encodes IL-2, IL-4, IL-7, and/or IL-15 and additionally or alternatively comprise a chimeric antigen receptor (CAR). In specific embodiments, the CAR is a CAR that targets the GD2 antigen, for example in neuroblastoma.

Abstract: Disclosed are a method and device for triggering protection switching by signal degrade of a link aggregation port, wherein the method includes: acquiring status information of member ports of a link aggregation port from a status register of the link aggregation port; obtaining a number value X of member ports of the link aggregation port which generate signal degrade light path attenuation according to the acquired status information of the member ports; comparing the obtained number value X with a predetermined threshold value; and when the number value X is greater than the predetermined threshold value, setting statuses of all the member ports of the link aggregation port to be a signal degrade status, and notifying a virtual section layer to report fault and perform a service protection switching to a backup link.

Abstract: Disclosed are a method and device for triggering protection switching by signal degrade of a link aggregation port, wherein the method includes: acquiring status information of member ports of a link aggregation port from a status register of the link aggregation port; obtaining a number value X of member ports of the link aggregation port which generate signal degrade light path attenuation according to the acquired status information of the member ports; comparing the obtained number value X with a predetermined threshold value; and when the number value X is greater than the predetermined threshold value, setting statuses of all the member ports of the link aggregation port to be a signal degrade status, and notifying a virtual section layer to report fault and perform a service protection switching to a backup link.

Abstract: The present invention regards methods and/or compositions related to Natural Killer T cells that are engineered to harbor an expression construct that encodes IL-2, IL-4, IL-7, and/or IL-15 and additionally or alternatively comprise a chimeric antigen receptor (CAR). In specific embodiments, the CAR is a CAR that targets the GD2 antigen, for example in neuroblastoma.