Evidence map›Paper›PMID 41875099›Full record

ArticlePLoS biology2026

Disrupting CD22-cis-ligand interactions ameliorates type 1 diabetes and graft rejection by expanding regulatory B cells.

Wang Long, Ayaka Endo, Hashadi Nadeesha Walakulu Gamage, Tianyi Yang, Toru Suzuki, Takeshi Nitta, Hiromu Takematsu, Kenya Honda, Masatake Asano, Takeshi Tsubata

Abstract read
In one paragraph

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

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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

10 authors.

Wang LongDepartment of Pathology, Nihon University School of Dentistry, Chiyoda-ku, Tokyo, Japan.
Ayaka EndoDepartment of Immunology, Medical Research Laboratory, Institute of Integrated Research, Institute of Science Tokyo, Bunkyo-ku, Tokyo, Japan.
Hashadi Nadeesha Walakulu GamageDepartment of Pathology, Nihon University School of Dentistry, Chiyoda-ku, Tokyo, Japan.
Tianyi YangDepartment of Immunology, Medical Research Laboratory, Institute of Integrated Research, Institute of Science Tokyo, Bunkyo-ku, Tokyo, Japan.
Toru SuzukiLaboratory of Genome Editing for Biomedical Research, Medical Research Laboratory, Institute of Science Tokyo, Bunkyo-ku, Tokyo, Japan.
Takeshi NittaDivision of Molecular Pathology, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda, Chiba, Japan.
Hiromu TakematsuDepartment of Molecular Cell Biology, School of Medical Sciences, Fujita Health University, Toyoake, Aichi, Japan.
Kenya HondaDepartment of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Masatake AsanoDepartment of Pathology, Nihon University School of Dentistry, Chiyoda-ku, Tokyo, Japan.
Takeshi TsubataDepartment of Pathology, Nihon University School of Dentistry, Chiyoda-ku, Tokyo, Japan.ORCID https://orcid.org/0000-0003-0760-1258

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD22 is an inhibitory receptor expressed in B cells and is constitutively associated with α2,6-sialylated membrane proteins expressed on the same cell (cis-ligands). However, interaction with cis-ligands is required for the function of CD22 only in part. To address the role of ligand interaction of CD22 in immune responses, here we generated anti-CD22 antibody 1C5 that specifically inhibits ligand binding of CD22. Both Cd22-/- mice and mice treated with 1C5 show expansion of regulatory B (Breg) cells in follicular (FO) B cells, suggesting a crucial role of ligand interaction of CD22 in inhibiting the expansion of FO Breg cells. CD22 appears to recognize BCR and TLRs thereby directly or indirectly suppressing TLR signaling essential for expansion of Breg cells. Treatment of mice with 1C5 ameliorates skin graft rejection and type 1 diabetes with expansion of regulatory γδ T cells probably through expansion of Breg cells, suggesting ligand interaction of CD22 as a novel target of therapy for autoimmune diseases and graft rejection.

Indexed as

B-Lymphocytes, RegulatoryDiabetes Mellitus, Type 1Graft RejectionSialic Acid Binding Ig-like Lectin 2AnimalsLigandsMiceMice, Inbred C57BLMice, KnockoutSignal TransductionSkin TransplantationCd22 protein, mouseLigandsSialic Acid Binding Ig-like Lectin 2

Identifiers

PMID41875099
PMCPMC13012520

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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.