Related Experiment Video
Updated: May 13, 2026

05:03
Accessing Early Differentiation of Virus-Specific Follicular Helper CD4+ T Cell in Acute LCMV-Infected Mice
Published on: April 26, 2024
A Functional TNFRSF13B Variant Disrupts B-Cell Enhancer Activity and Increases Susceptibility to EBV-Negative
Julia Nakano1, Nguyen Hoang Viet2, Hoang Thao Giang Nguyen1
1Faculty of Health Sciences, Kanazawa University, Kanazawa, Japan.
Gene
|May 11, 2026
Summary
A specific gene variant (rs4792800 GG genotype) in TNFRSF13B increases lymphoma risk, particularly for diffuse large B-cell lymphoma and EBV-negative cases. This suggests inherited immune regulation defects contribute to cancer development.
Area of Science:
- Genetics
- Immunology
- Oncology
Background:
- The TNFRSF13B gene encodes TACI, crucial for B-cell survival and immune homeostasis.
- Gene variants are linked to immunodeficiency, but their role in lymphoma is not fully understood.
Purpose of the Study:
- To investigate the association between the TNFRSF13B polymorphism rs4792800 (A>G) and lymphoma risk.
Main Methods:
- A hospital-based case-control study with 200 lymphoma patients and 119 healthy controls.
- Genotyping using allele-specific PCR and logistic regression analysis.
- In silico analysis to assess regulatory potential and transcription factor binding.
Main Results:
- The G allele was significantly more common in lymphoma cases (51.8%) than controls (42.0%).
- The rs4792800 GG genotype showed a 1.9-fold increased lymphoma risk, especially in diffuse large B-cell lymphoma (OR=2.32) and EBV-negative disease (OR=1.99).
- In silico analysis indicated the G allele disrupts EBF1 binding and enhances PAX5 binding, potentially reducing TNFRSF13B expression.
Conclusions:
- The rs4792800 GG genotype is linked to a higher risk of developing lymphoma.
- Inherited variations affecting TACI-mediated immune surveillance may contribute to lymphomagenesis independently of viral factors.
More Related Videos
Related Concept Videos
T Cell Types and Functions
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
NF-κB-dependent Signaling Pathway
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
B Cell Activation and Differentiation
The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...
Abnormal Proliferation
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...

