---
title: "B cell receptor signaling drives ERV-associated lymphomagenesis in T-cell–deficient B6-Ly5.1 mice"
id: "pubmed-42275834"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42275834"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42275834/"
doi: "10.1016/j.bbrc.2026.154139"
published_at: "2026-08-27T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# B cell receptor signaling drives ERV-associated lymphomagenesis in T-cell–deficient B6-Ly5.1 mice
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42275834
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42275834/)
- **DOI:** [10.1016/j.bbrc.2026.154139](https://doi.org/10.1016%2Fj.bbrc.2026.154139)
- **Published At:** 2026-08-27T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Endogenous retroviruses (ERVs) are normally epigenetically silenced but can be reactivated under immunodeficient conditions and contribute to tumorigenesis. - The study demonstrates that **B cell receptor (BCR) signaling** triggers reactivation of a specific ERV, **Emv10**, in T-cell-deficient B6-Ly5.1 mice. - Reactivation of Emv10 correlated with development of lethal B cell tumors that display a **germinal center B cell-like (GCL)** phenotype and show evidence of somatic hypermutation. - Tumors harbored recurrent endogenous murine leukemia virus (eMLV) proviral insertions near the **Plch2** locus on chromosome 4, associated with abnormal activation of **Plch2**. - Chronic in vivo antigen stimulation with NP-Ficoll markedly accelerated GCL development and systemic accumulation of malignant cells, indicating a role for chronic BCR engagement in promoting malignancy. - In a model where direct BCR stimulation targeted only a small subset of λ+ B cells, the accelerated tumors arose predominantly from non-stimulated λ- B cell clones, implying a **non-cell-autonomous** mechanism by which physiological BCR activation promotes lymphomagenesis. - Findings highlight a critical role for **T cell–mediated immune surveillance** in limiting ERV-driven tumor propagation across the host B cell compartment. - The study links physiological BCR activation, ERV reactivation (Emv10), proviral insertional mutagenesis (eMLV near Plch2), and loss of T cell surveillance as cooperating factors in B cell lymphomagenesis in this mouse model.
## Clinical Analysis & Structured Key Points
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Epub 2026 Jun 11. # B cell receptor signaling promotes endogenous retrovirus-associated lymphomagenesis in T-cell-deficient B6-Ly5.1 mice [Kagefumi Todo](https://pubmed.ncbi.nlm.nih.gov/?term=Todo+K&cauthor_id=42275834)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42275834/#full-view-affiliation-1 "Department of Health and Nutrition, Faculty of Human Sciences, Tokiwa University, 1-430-1, Miwa, Mito, Ibaraki, 310-8585, Japan. Electronic address: k-todo@tokiwa.ac.jp."), [Masaki Hikida](https://pubmed.ncbi.nlm.nih.gov/?term=Hikida+M&cauthor_id=42275834)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42275834/#full-view-affiliation-2 "Laboratory for Cellular Physiology, Department of Life Science, Graduate School of Engineering Science, Akita University, 1-1, Tegata-gakuencho, Akita, 010-8502, Japan.") Affiliations Expand ### Affiliations * 1 Department of Health and Nutrition, Faculty of Human Sciences, Tokiwa University, 1-430-1, Miwa, Mito, Ibaraki, 310-8585, Japan. Electronic address: k-todo@tokiwa.ac.jp. * 2 Laboratory for Cellular Physiology, Department of Life Science, Graduate School of Engineering Science, Akita University, 1-1, Tegata-gakuencho, Akita, 010-8502, Japan. * PMID: **42275834** * DOI: [ 10.1016/j.bbrc.2026.154139 ](https://doi.org/10.1016/j.bbrc.2026.154139) Item in Clipboard # B cell receptor signaling promotes endogenous retrovirus-associated lymphomagenesis in T-cell-deficient B6-Ly5.1 mice Kagefumi Todo et al. Biochem Biophys Res Commun. 2026. Show details Display options Display options Format Abstract PubMed PMID Biochem Biophys Res Commun Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Biochem+Biophys+Res+Commun%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Biochem+Biophys+Res+Commun%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42275834/) . 2026 Aug 27:828:154139. doi: 10.1016/j.bbrc.2026.154139. Epub 2026 Jun 11. ### Authors [Kagefumi Todo](https://pubmed.ncbi.nlm.nih.gov/?term=Todo+K&cauthor_id=42275834)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42275834/#short-view-affiliation-1 "Department of Health and Nutrition, Faculty of Human Sciences, Tokiwa University, 1-430-1, Miwa, Mito, Ibaraki, 310-8585, Japan. Electronic address: k-todo@tokiwa.ac.jp."), [Masaki Hikida](https://pubmed.ncbi.nlm.nih.gov/?term=Hikida+M&cauthor_id=42275834)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42275834/#short-view-affiliation-2 "Laboratory for Cellular Physiology, Department of Life Science, Graduate School of Engineering Science, Akita University, 1-1, Tegata-gakuencho, Akita, 010-8502, Japan.") ### Affiliations * 1 Department of Health and Nutrition, Faculty of Human Sciences, Tokiwa University, 1-430-1, Miwa, Mito, Ibaraki, 310-8585, Japan. Electronic address: k-todo@tokiwa.ac.jp. * 2 Laboratory for Cellular Physiology, Department of Life Science, Graduate School of Engineering Science, Akita University, 1-1, Tegata-gakuencho, Akita, 010-8502, Japan. * PMID: **42275834** * DOI: [ 10.1016/j.bbrc.2026.154139 ](https://doi.org/10.1016/j.bbrc.2026.154139) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID ## Abstract Endogenous retroviruses (ERVs) are typically epigenetically silenced but can contribute to tumorigenesis upon reactivation under immunodeficient conditions. However, the precise physiological triggers and microenvironmental mechanisms driving ERV-mediated oncogenesis in vivo remain poorly understood. Here, we demonstrate that B cell receptor (BCR) signaling triggers ERV (specifically Emv10) reactivation and promotes lymphomagenesis in T cell-deficient B6-Ly5.1 mice. The resulting tumors exhibited a distinct germinal center B cell-like (GCL) phenotype with somatic hypermutations and harbored recurrent eMLV proviral insertions near the Plch2 locus on chromosome 4, associated with aberrant activation of Plch2. In vivo, chronic antigen stimulation with NP-Ficoll significantly accelerated lethal GCL development, accompanied by systemic accumulation of malignant cells. Crucially, in a model where direct BCR stimulation was restricted to a minor subset of λ+ B cells, the accelerated malignancies arose predominantly from non-stimulated λ- B cell clones. These findings suggest that physiological BCR activation may promote lymphomagenesis through a non-cell-autonomous mechanism. Our model highlights a novel, vital role for T cell-mediated immune surveillance in restricting ERV-driven tumor propagation across the host B cell compartment. **Keywords:** B cell receptor; Endogenous retrovirus (ERV); Germinal center B cells; Immune surveillance; Lymphomagenesis. Copyright © 2026 Elsevier Inc. All rights reserved. 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