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T-cell activation against multiple patient-specific lymphoma antigens

Molecular classification
Other
01

Overview

This entry describes a therapeutic approach, not a molecule: T-cell activation against multiple patient-specific lymphoma antigens refers to strategies—most notably, CAR T-cell therapies—where T cells (often from the patient) are engineered or directed to recognize and attack lymphoma cells expressing a variety of antigens that are unique to or highly expressed in that patient's tumor. Unlike classical drug targets (such as a single receptor or enzyme), this process leverages both natural and synthetic immune recognition elements (TCR or CAR) to trigger cytotoxic T-cell responses, aiming to overcome immune evasion by lymphomas through multi-antigen targeting or personalized antigen selection. This field's clinical impact has been demonstrated in several hematological malignancies, particularly B-cell lymphomas, using CAR T cells with anti-CD19 and anti-CD22 specificity among others. Key safety challenges include life-threatening cytokine release syndrome and tumor escape if targeted antigens are lost or downregulated by the tumor.

Other names
patient-specific T-cell lymphoma antigen responselymphoma antigen-directed T-cell activationmulti-antigen-specific T-cell response in lymphoma
02

Mechanism of action

Not a single molecule, but general mechanisms involve: T-cell receptor/CAR binding to antigen on lymphoma cell → T-cell activation → cytotoxicity via perforin/granzyme or death receptor pathways; Enhanced cytokine secretion and immune synapse formation; Overcoming immunosuppression or immune evasion mechanisms by tumor cells, including antigen loss, T-cell exhaustion, and inhibitory signals (PD-1/PD-L1, LAG-3, TGF-β).

03

Biological functions

Immune responseAntigen recognitionCytotoxicityImmunosurveillanceTumor cell killing
04

Disease associations

Cancerlymphoma (B-cell lymphoma, diffuse large B-cell lymphoma, follicular lymphoma, Hodgkin lymphoma, etc.)
05

Safety considerations

Cytokine release syndromeneurotoxicity (ICANS)antigen escape (tumor cells losing or reducing target antigen)T-cell exhaustionimmunosuppressionrisk of severe infection due to B-cell aplasia or lymphodepletion
06

Interacting drugs

tisagenlecleucel

5 more in the full profile.

07

Biomarkers

Lymphoma surface antigens targeted by therapy (e.g., CD19, CD20, CD22, BCMA depending on context)Cytokine profiles (e.g., IL-6 for monitoring cytokine release syndrome)Tumor mutation burden, antigen expression/histology for predicting response/resistance

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