Humanized antibodies, capable of specific binding to human CEACAM1 molecules containing human-to-murine back-mutations in non-CDR variable regions, and their encoding polynucleotide sequences are provided. Pharmaceutical compositions comprising these antibodies as well as methods of their use in treating and diagnosing cancer and other conditions are also provided.

The present invention relates to a chimeric antigen receptor including a CD30-derived intracellular signaling domain, immune cells expressing same, and uses thereof. More specifically, the present invention is designed to use a chimeric antigen receptor including a portion of the sequence of TRAF-binding domain within the CD30 domain as an intracellular signaling domain to increase the proliferation and survival of immune effector cells, thereby providing an effect of enhancing antitumor efficacy and cytokine secretion.

SIRP1alpha-41BBL fusion proteins are provided. Accordingly, there is provided a SIRPalpha-41BBL fusion protein comprising a single amino acid linker between the SIRPalpha and the 41BBL. Also there is provided a SIRPalpha-41BBL fusion protein in a form of at least a homo-trimer. Also provided are polynucleotides and nucleic acid constructs encoding the SIRP1alpha-41BBL fusion protein, host-cells expressing the SIRP1alpha-41BBL fusion protein and methods of use thereof.

This document provides methods and materials involved in treating a mammal (e.g., a human) having (or risk of developing) graft-versus-host disease (GVHD). For example, T cells (e.g., regulatory T cells) expressing one or more antigen receptors targeting one or more epithelial-specific antigens are provided. Also provided are methods for administering T-cells expressing one or more antigen receptors targeting one or more epithelial-specific antigens to a mammal having (or at risk of developing) GVHD to treat the GVHD.

A chimeric polypeptide, containing a binding peptide that can specifically bind to a target molecule, a receptor regulatory domain containing one or more cleavage sites, and an intracellular domain. The receptor regulatory domain comprises an extracellular region and a transmembrane region, wherein the extracellular region and the transmembrane region are not both derived from a Notch protein. The binding of the binding peptide to the target molecule can induce the cleavage of the receptor regulatory domain, thereby releasing the intracellular domain.

The present disclosure relates to cell therapy methods for treating solid carcinoma tumors comprising administration of immune cells expressing a chimeric antigen receptor (CAR) comprising a mutant I domain of the .sub.L subunit of human lymphocyte function-associated antigen-1 (LFA-1), which are cytotoxic against solid carcinoma tumors overexpressing ICAM-1 and alleviate on-target, off-tumor toxicities.

SIRP1alpha-41BBL fusion proteins are provided. Accordingly, there is provided a SIRPalpha-41BBL fusion protein comprising a single amino acid linker between the SIRPalpha and the 41BBL. Also there is provided a SIRPalpha-41BBL fusion protein in a form of at least a homo-trimer. Also provided are polynucleotides and nucleic acid constructs encoding the SIRP1alpha-41BBL fusion protein, host-cells expressing the SIRP1alpha-41BBL fusion protein and methods of use thereof.

An immune cell with down-regulated cell adhesion capability and the medical use thereof. The immune cell is a tumor killer cell for adoptive immune cell therapy, and has down-regulated cell adhesion capability. The immune cell has better safety for hematological tumors and solid tumors.

An anti-CD371 (anti-CLL-1) chimeric antigen receptor (CAR), engineered immune cells comprising the CAR, as well as therapeutic compositions, therapeutic methods and companion diagnostic methods are disclosed herein.

Methods of using soluble tandem selectin glycoprotein ligand (TSGL) and TSGL fusion proteins, such as TSGL-Ig, for therapeutic treatment of cancers, including in combination with T cell activation therapies or an adoptive cell transfer (ACT) therapy.