Evidence map›Paper›PMID 42191836›Full record

ArticleScientific reports2026

CD80 (B7-1) as a potential therapeutic target in Epstein-Barr virus‑associated B cell diseases.

Rin Yoshizato, Mariko Miura, Yumi Tamura, Yohei Kawano, Yuya Hokama, Nanami Soda, Yusei Ota, Kotomi Yamashita, Taisei Fukushima, Masataka Ishimura and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Rin YoshizatoDepartment of Immunology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Mariko MiuraDepartment of Immunology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Yumi TamuraDepartment of Immunology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Yohei KawanoDepartment of Immunology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Yuya HokamaDepartment of Immunology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Nanami SodaDepartment of Immunology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Yusei OtaDepartment of Immunology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Kotomi YamashitaDepartment of Immunology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Taisei FukushimaDepartment of Immunology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Masataka IshimuraDepartment of Pediatrics, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Shouichi OhgaDepartment of Pediatrics, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Tomoharu YasudaDepartment of Immunology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan. yasudat@hiroshima-u.ac.jp.

Funding

Japan Agency for Medical Research and Development 18ek0109334h0001, 19ek0109334h0002, 20ek0109334h0003, 22ek0109609h0001, 23ek0109609h0002, 22ek0109612h0001, and 23ek0109612h0002Japan Agency for Medical Research and Development JP20fk0108453Japan Science and Technology Agency JPMJPF2010, JPMJSFS1A8Japan Society for the Promotion of Science JP21H02751Japan Society for the Promotion of Science JP24K11047Natural Science Center for Basic Research and Development, Hiroshima University NBARD-00134
6 · The paper itself

Abstract

Epstein-Barr virus (EBV)-associated B-cell lymphomas pose a therapeutic challenge due to their resistance to conventional chemotherapy and limited efficacy of current targeted approaches. Here, we identified CD80 as a cell surface antigen highly expressed in EBV-positive B-cell lymphomas. Monoclonal antibodies were generated from mice immunized with recombinant human CD80 and subsequently engineered into chimeric formats. These antibodies were evaluated for their cytotoxic activity against CD80-expressing lymphoma cells. Notably, high-affinity clones elicited robust antibody-dependent cellular cytotoxicity (ADCC) but lacked complement-dependent cytotoxicity (CDC), in contrast to rituximab, which targets CD20 and mediates both ADCC and CDC. Our findings suggest that cytotoxic effector functions are regulated not only by the constant region of the antibody but also by the antigen recognized by its variable region. Importantly, these CD80-specific antibodies do not inhibit T cell responses against EBV-positive immortalized cells, highlighting their potential as promising therapeutic candidates for EBV-positive lymphomas and other CD80-expressing malignancies.

Indexed as

B7-1 AntigenEpstein-Barr Virus InfectionsHerpesvirus 4, HumanLymphoma, B-CellAnimalsAntibodies, MonoclonalAntibody-Dependent Cell CytotoxicityCell Line, TumorHumansMiceRituximabAntibodies, MonoclonalB7-1 AntigenRituximab

Identifiers

PMID42191836
PMCPMC13438696

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.