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- W2032341321 abstract "•Immune evasion is a limiting factor for the success of many cancer immunotherapies. •Recombinant fusion proteins can circumvent many tumor immune escape mechanisms. •Various T cell activating bispecific constructs have shown success in clinics. •Immunoligands targeting NK cells are promising therapeutic tools for cancer patients. The insight that the immune system is able to eradicate tumor cells inspired the development of targeted immunotherapies. These novel approaches aim to trigger immune molecules and receptors, including CD3 on T cells and NKG2D and NKp30 on natural killer (NK) cells, to harness the immune system against cancer. In cancer patients, overcoming immune suppression induced by malignant cells or by the tumor microenvironment remains the major challenge to the clinical efficacy of immunotherapies. Recombinant constructs have been developed in various formats either utilizing natural ligands (immunoligands) or antibody-derived components (immunoconstructs) to circumvent mechanisms that counteract an effective antitumor immune response. The insight that the immune system is able to eradicate tumor cells inspired the development of targeted immunotherapies. These novel approaches aim to trigger immune molecules and receptors, including CD3 on T cells and NKG2D and NKp30 on natural killer (NK) cells, to harness the immune system against cancer. In cancer patients, overcoming immune suppression induced by malignant cells or by the tumor microenvironment remains the major challenge to the clinical efficacy of immunotherapies. Recombinant constructs have been developed in various formats either utilizing natural ligands (immunoligands) or antibody-derived components (immunoconstructs) to circumvent mechanisms that counteract an effective antitumor immune response. transfer of T/NK cells derived from the host itself (autologous) or from a donor (allogeneic) to deliver particular effector functions associated with respective cells. For example, autologous transfer of tumor infiltrating lymphocytes (TILs) to treat solid malignancies or allogeneic transfer of NK cells (from a haploidentical donor) to combat leukemia. a defense mechanism governed by interaction between the Fc regions of antibodies and Fc receptors on certain immune cells such as NK cells, macrophages, neutrophils, and eosinophils to actively lyse infectious agents, infected cells, and malignant cells. ADCC is a mode of adaptive immune response as its activation is dependent upon presence of target-specific antibodies (humoral immunity). For antibody-derived agents lacking an Fc domain the term ‘redirected lysis’ is used with similar meaning. a recombinant protein containing two arms with two different specificities – generally one for a target cell (e.g., tumor cell) and the other for an effector cell (e.g., NK cell). Many different formats of bispecific constructs exist including bispecific antibodies (bsAbs), bispecific scFvs (bs-scFvs), diabodies, etc. receptors with specificities for Fc region of IgG antibodies that belong to the immunoglobulin superfamily. Different members of FcγRs include FcγRI (CD64), FcγRIIA/B (CD32a/b), and FcγRIIIA/B (CD16a/b), which differ in their affinities for Fc region of IgG; for example, FcγRI binds more strongly to antibody compared with FcγRII or FcγRIII. a transmembrane receptor from the immunoglobulin (Ig) superfamily with low affinity for the Fc domain of the IgG subclass. It is mostly expressed on NK cells and at low levels on macrophages (certain tissue types) and associates with ITAM (immunoreceptor tyrosine-based activation motif)-containing domains for activation of respective cells. the Fc region is the tail or base part of an antibody and is composed of two heavy chains containing either two or three constant domains depending upon the class of the antibody. The Fc region mediates antibody-dependent immune cell and complement activation by binding to surface receptors, such as Fc receptors, and complement proteins. transplantation of hematopoietic stem cells (HSCs) from partially HLA-matched donors (patient relatives) into patients (generally hematological cancer patients) for whom an HLA-identical sibling or a matched unrelated donor is not available. a family of germ-line encoded trans-membrane receptors of the immunoglobulin superfamily that are expressed on NK cells. NKp30, NKp44, and NKp46 comprise an extracellular ligand-binding domain and a transmembrane domain but lack any intracellular signaling domain. Upon stimulation, these receptors associate with appropriate adaptor proteins to propagate signaling and activate NK cells. an activating receptor from the C-type lectin-activating receptor family and expressed on all human NK cells and CD8+ T cells. In humans, it associates with a homodimer of the YINM motif harboring adaptor protein DAP10 (DNAX-activating protein 10) for activation of respective cells. a member of the group of NCRs from the immunoglobulin superfamily, expressed on human NK cells where it associates with the ITAM containing domains for NK cell activation. a protein comprising variable domains of heavy (VH) and light (VL) immunoglobulin chains fused to each other by a short glycine and serine rich linker. This monoclonal antibody-derived fusion protein retains the specificity of its parent antibody but lacks the Fc domain and related effector functions. enhanced NK cell activation by simultaneous ligation of two or more specific activating receptors on NK cells that is higher compared with simple additive effects from stimulation by each receptor (co-stimulation). For example, (i) co-stimulation of receptor A and B can be described as: A + B = AB (additive effects); (ii) synergy between receptor A and B can be described as: A + B > AB (synergistic effects). a recombinant protein containing three arms with different or overlapping specificities – generally two arms specific for the same antigen (monotargeting construct) or distinct antigens (dual-targeting construct) on a target cell (e.g., tumor cell) and a third arm is specific for an effector cell (e.g., NK cell). a process/mechanism by which tumor variants with low immunogenicity escape active tumor immunosurveillance by ignoring, tolerating, and attacking the immune system. a process/mechanism by which the immune system identifies and kills nascent transformed cells before they fully acquire cancerous potential." @default.
- W2032341321 created "2016-06-24" @default.
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- W2032341321 date "2014-02-01" @default.
- W2032341321 modified "2023-09-23" @default.
- W2032341321 title "Natural ligands and antibody-based fusion proteins: harnessing the immune system against cancer" @default.
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- W2032341321 doi "https://doi.org/10.1016/j.molmed.2013.10.006" @default.
- W2032341321 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24268686" @default.
- W2032341321 hasPublicationYear "2014" @default.
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