Recommended Information


In vitro–differentiated Th1/Th17/Treg cells

CD4+ helper T cells (Th cells) serve as mediators of cellular immunity and play a critical role in activating other immune cells, such as B cells and cytotoxic T cells, as well as in regulating immune responses.

Antibody-Dependent Cell-Mediated Cytotoxicity Assay (ADCC)

Antibodies, as integral components of the immune system, play a crucial role in defending against disease. Antibody-dependent cell-mediated cytotoxicity (ADCC) is one of the mechanisms by which antibodies exert their effector functions: when IgG antibodies specifically bind via their Fab fragments to antigenic epitopes on the surface of target cells—such as virus-infected cells and tumor cells—the Fc portion of the antibody can engage Fc receptors on effector cells, including natural killer (NK) cells, monocytes–macrophages, and neutrophils, thereby triggering the effector cells’ cytotoxic activity and directly killing the target cells. The ability to elicit ADCC against target cells is an important functional criterion for antibody candidates that are directed against cancer-associated antigens.

Antibody-dependent cellular phagocytosis

Antibody-dependent cellular cytotoxicity (ADCC) is one of the mechanisms by which antibody-based therapies exert their antitumor and other therapeutic effects. Currently, therapeutic strategies aimed at enhancing macrophage responses to therapeutic antibodies have garnered significant attention from researchers, including the identification of novel targets and the development of antibodies with enhanced functionality.

Complement-dependent cytotoxicity (CDC)

Complement is a group of heat-labile, enzymatically active proteins found in human and vertebrate serum and tissue fluids, comprising more than 30 soluble and membrane-bound proteins. Complement-dependent cytotoxicity (CDC) refers to the lytic effect on target cells resulting from the formation of a membrane attack complex after complement is activated by specific antibodies that bind to corresponding antigens on the cell membrane via the classical pathway of complement activation. Initially, antibodies bind to complement component C1q, which then triggers the sequential activation of C2 through C9 to form the membrane attack complex, ultimately leading to lysis of the target cell.

Cytokine Release Syndrome Risk Assessment (CRS)

Cytokine release syndrome (CRS) refers to a hyperactive immune response that occurs following infection with pathogenic microorganisms, leading to the rapid activation of numerous immune cells and the massive release of multiple cytokines—including TNF-α, IL-1, IL-6, IL-12, IFN-α, IFN-β, and IFN-γ—within a short period. This results in a severe systemic inflammatory response syndrome. The excessive production of these cytokines can damage tissues and organs, thereby giving rise to a wide range of clinical manifestations. Currently, the standard approach is to closely monitor and target the specific cytokines that trigger the cytokine storm.

Introduction to Neutralizing Antibodies Against Authentic Viruses

Currently, pseudovirus-based assays closely mimic physiological infection mechanisms and can largely replicate the in vivo therapeutic efficacy; however, there is a substantial discrepancy between neutralization assay results obtained with live viruses and those obtained with pseudoviruses. Therefore, live-virus neutralization assays are an indispensable step in the development of antiviral drugs and vaccines.

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RCL detection

In CAR-T cell manufacturing, most retroviruses and lentiviruses used for cellular gene therapy are engineered as replication-deficient viral vectors and are co-transfected using multiple plasmids to express the lentivirus or γ-retrovirus. During production, homologous recombination may occur between the deleted vector backbone and wild-type viral sequences, leading to the generation of replication-competent virus (RCL), which poses a serious risk to human health. Therefore, RCL testing is one of the most critical components of safety assessment.

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