Provided is an engineered immune cell. The cell expresses a chimeric antigen receptor comprising an antigen-binding region. The antigen-binding region comprises an anti-CD7 antibody, and the expression of endogenous CD7, at least one TCR/CD3 gene, and at least one MHC-II related gene is suppressed or silenced. Further provided is the use of the engineered immune cell in the treatment of diseases associated with CD7 expression.

The present disclosure relates to an engineered immune cell and use thereof. The present disclosure provides an engineered immune cell comprising a CAR or engineered TCR, which CAR or engineered TCR can comprise a first antigen binding domain and a second antigen binding domain. The engineered immune cells of the present disclosure, when administered into a subject, can inhibit the host immune cells such as T cells and/or NK cells and enhance the survival and persistence of the engineered immune cells in vivo, thereby exhibiting more effective tumor killing activity.

A chimeric antigen receptor is disclosed that includes: (a) an scFv comprising a light chain variable domain (V.sub.L) and a heavy chain variable domain (V.sub.H), wherein the scFv specifically binds to CCR4; (b) a hinge and transmembrane domain from CD8; (c) an intracellular 4-1BB signaling domain; and (d) an intracellular CD3 zeta signaling domain, wherein (a)-(d) are in N to C terminal order. Uses of the chimeric antigen receptor, such as for treating a malignancy, are also disclosed.

Provided herein are acute myeloid leukemia antigen targets for chimeric receptors and methods of using same.

Provided herein are uses of chimeric antigen receptors (CARs) for treating a tumor or a cancer (such as B cell related cancer, e.g., multiple myeloma). In addition, an optimal washout period for commencing a therapy for the treatment of a condition in a subject after a prior exposure can be determined by receiving, for each of a plurality of subjects, prior treatment history data. Left-censored data can then be derived from the prior treatment history data for each of the subjects that includes a washout period and event or censor. A time scale of the left-censored treatment data is then inverted to result in right-censored treatment data. The right-censored treatment data is then applied to a time-to-event (TTE) model that associates one or more variables of interest with a time since exposure to the prior exposure. A maximally selected log-rank statistic across a plurality of cutoffs within a pre-defined percentile range is computed for continuous variables within the one or more variables of interest. One or more variables and associated cutoffs for the continuous variables having a maximally selected log-rank statistic below a first pre-defined threshold are then identified. A test statistic of each (n−1) strata relative to a reference stratum is then computed for ordinal or categorical variables within the one or more variables of interest. One or more ordinary or categorical variables and associated strata having a test statistic below a second pre-defined threshold, relative to the reference stratum are identified. An optimal washout period is then determined for the therapy based on the cutoff having a lowest value below the pre-defined threshold and relative to a median of subject values below the pre-defined threshold and a median of subject values above the pre-defined threshold.

Provided herein are binding proteins recognizing HA-1 antigen and uses thereof.

A method of treating a Philadelphia chromosome-positive tumor in a subject comprises administering to the subject a therapeutic composition comprising an incubated combined mixture of (a) a first component comprising (i) Philadelphia chromosome-positive tumor lysate, (ii) plasmid encoding bcr/abl fusion protein, or (iii) bcr/abl fusion peptide; and (b) a second component comprising plasmacytoid dendritic cells expressing Toll-like receptor 9 and modified for stable expression of CD40 ligand or GM-CSF by a nucleotide sequence engineered into said plasmacytoid dendritic cells.

The disclosure is directed to methods and compositions relating to genetically engineered cells expressing chimeric antigen receptors, where the cells are mobilized lymphocytes.

The present disclosure relates to treating a subject comprising administering to the subject a therapy (e.g., a cell therapy, e.g., an adoptive cell therapy, e.g., a CAR-T cell therapy), wherein, prior to the administration, the subject has been preconditioned with a personalized amount of a chemotherapeutic agent. The personalized amount provides an optimal exposure to the chemotherapeutic agent.

The present application provides an anti-CD5 antibody. The present application further provides a chimeric antigen receptor (CAR) that specifically binds to a CD5 protein, which comprises a CD5 binding domain, a transmembrane domain, a co-stimulatory domain and an intracellular signaling domain. Further provided are engineered immune effector cells (such as T-cells) comprising the chimeric antigen receptor. The present application further provides use of the CAR and the engineered immune effector cells in the treatment of diseases or conditions associated with the expression of CD5.