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Tumor-associated antigen recognized by cytokine-induced killer cell effector mechanisms

Molecular classification
Other, Peptide antigens
01

Overview

Cytokine-induced killer (CIK) cells are a heterogeneous immune cell population with features of both T lymphocytes (CD3+) and NK-like effectors (CD56+), capable of MHC-restricted and MHC-unrestricted killing of tumor cells through recognition of diverse tumor-associated antigens. These antigens encompass any molecular marker (peptide or otherwise) expressed preferentially on malignant cells, many of which are recognized via NKG2D, DNAM-1, NKp30, or redirected recognition by engineered TCRs or CARs. The term as written does not indicate a singular molecule but rather highlights the unique capacity of CIK cells to engage and lyse tumor cells through multiple antigen recognition mechanisms, both innate and adaptive. This entry is not a canonical, single molecular target but a functional classification referring to a broad spectrum of tumor antigens recognized by unique CIK cell effectors. For any actionable target data, a specific antigen (e.g., "NY-ESO-1", "CD19", "EGFR") must be selected. This term should be corrected or replaced with the specific antigen of interest to facilitate structured data organization.

Other names
TAAs recognized by CIK cellsTumor antigens for CIK recognitionAntigens targeted by T/NK-like killing by CIK cells
02

Mechanism of action

Cell-mediated cytotoxicity (mainly via NKG2D- or TCR-dependent recognition); Antibody-dependent cell-mediated cytotoxicity (ADCC, when combined with monoclonal antibodies through CD16a engagement); MHC-unrestricted tumor cell killing

03

Biological functions

Immune recognitionImmune responseTumor cell killingAntigen presentation
04

Disease associations

Cancer
05

Safety considerations

Off-tumor cytotoxicity (if redirected to widely-expressed antigens)Cytokine release syndrome (less frequent than with CAR-T cells)Graft-versus-host disease (GVHD)—very low compared to allogeneic T cells
06

Biomarkers

Expression of NKG2D ligands on tumor cells (e.g., MICA/B, ULBP family for NKG2D-mediated recognition)Presence of specific tumor-associated peptide antigens for TCR/CAR redirectionCell surface antigens such as CD19, CD20, EGFR, Her2 (when CIK cells are redirected by bispecific antibodies or CAR constructs)

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