Evidence map›Paper›PMID 37490914›Full record

ArticleCell reports. Medicine2023

An agonistic anti-signal regulatory protein α antibody for chronic inflammatory diseases.

Markus M Xie, Bingbing Dai, Jason A Hackney, Tianhe Sun, Juan Zhang, Janet K Jackman, Surinder Jeet, Ricardo A Irizarry-Caro, Yongyao Fu, Yuxin Liang and 13 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports. Medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
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

17 citing papers in PubMed, 19 citations in OpenAlex.

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  8. Loss of NR2F6 Protects from Salmonella Typhimurium Infection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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

23 authors at 4 institutions in 3 countries.

Markus M XieDepartment of Immunology Discovery, Genentech, Inc., South San Francisco, CA, USA.
Bingbing DaiDepartment of Immunology Discovery, Genentech, Inc., South San Francisco, CA, USA.
Jason A HackneyDepartment of OMNI Biomarker Development, Genentech, Inc., South San Francisco, CA, USA.
Tianhe SunDepartment of Immunology Discovery, Genentech, Inc., South San Francisco, CA, USA.
Juan ZhangDepartment of Translational Immunology, Genentech, Inc., South San Francisco, CA, USA.
Janet K JackmanDepartment of Immunology Discovery, Genentech, Inc., South San Francisco, CA, USA.
Surinder JeetDepartment of Translational Immunology, Genentech, Inc., South San Francisco, CA, USA.
Ricardo A Irizarry-CaroDepartment of Immunology Discovery, Genentech, Inc., South San Francisco, CA, USA; Department of Human Pathobiology and OMNI Reverse Translation, Genentech, Inc., South San Francisco, CA, USA.
Yongyao FuDepartment of Discovery Oncology, Genentech, Inc., South San Francisco, CA, USA.
Yuxin LiangDepartment of Microchemistry, Proteomics, and Lipidomics and Next Generation Sequencing, Genentech, Inc., South San Francisco, CA, USA.
Hannah BenderDepartment of Pathology, Genentech, Inc., South San Francisco, CA, USA.
Eliah R ShamirDepartment of Pathology, Genentech, Inc., South San Francisco, CA, USA.
Mary E KeirDepartment of Human Pathobiology and OMNI Reverse Translation, Genentech, Inc., South San Francisco, CA, USA.
Jack BeversDepartment of Antibody Engineering, Genentech, Inc., South San Francisco, CA, USA.
Gerald NakamuraDepartment of Antibody Engineering, Genentech, Inc., South San Francisco, CA, USA.
Michael J TownsendDepartment of Human Pathobiology and OMNI Reverse Translation, Genentech, Inc., South San Francisco, CA, USA.
David A FoxDivision of Rheumatology, Clinical Autoimmunity Center of Excellence, University of Michigan Medical School, Ann Arbor, MI, USA.
Alexis ScherlDepartment of Pathology, Genentech, Inc., South San Francisco, CA, USA.
Wyne P LeeDepartment of Translational Immunology, Genentech, Inc., South San Francisco, CA, USA.
Flavius MartinDepartment of Immunology Discovery, Genentech, Inc., South San Francisco, CA, USA.
Paul J GodowskiDepartment of Immunology Discovery, Genentech, Inc., South San Francisco, CA, USA. Electronic address: godowski89@gmail.com.
Rajita PappuDepartment of Immunology Discovery, Genentech, Inc., South San Francisco, CA, USA. Electronic address: Pappu.Rajita@gene.com.
Tangsheng YiDepartment of Immunology Discovery, Genentech, Inc., South San Francisco, CA, USA. Electronic address: tangshengy@gmail.com.
Gene Therapy Laboratory · FRDiscovery Centre · CADiscovery Laboratories (United States) · USUniversity of Michigan · US

Funding

University of Michigan Clinical Autoimmunity Center of ExcellenceUM1AI144298 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FOX, DAVID ALAN, KHANNA, DINESH · 2019 to 2023
$546k
University of Michigan Autoimmunity Center of Excellence, Clinical Research ProgrUM1AI110557 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FOX, DAVID ALAN · 2014 to 2018
$543k
NIAID NIH HHS UM1 AI110557NIAID NIH HHS UM1 AI144298
6 · The paper itself

Abstract

Signal regulatory protein (SIRPα) is an immune inhibitory receptor expressed by myeloid cells to inhibit immune cell phagocytosis, migration, and activation. Despite the progress of SIRPα and CD47 antagonist antibodies to promote anti-cancer immunity, it is not yet known whether SIRPα receptor agonism could restrain excessive autoimmune tissue inflammation. Here, we report that neutrophil- and monocyte-associated genes including SIRPA are increased in inflamed tissue biopsies from patients with rheumatoid arthritis and inflammatory bowel diseases, and elevated SIRPA is associated with treatment-refractory ulcerative colitis. We next identify an agonistic anti-SIRPα antibody that exhibits potent anti-inflammatory effects in reducing neutrophil and monocyte chemotaxis and tissue infiltration. In preclinical models of arthritis and colitis, anti-SIRPα agonistic antibody ameliorates autoimmune joint inflammation and inflammatory colitis by reducing neutrophils and monocytes in tissues. Our work provides a proof of concept for SIRPα receptor agonism for suppressing excessive innate immune activation and chronic inflammatory disease treatment.

Indexed as

ColitisNeoplasmsHumansInflammationNeutrophilsPhagocytosisagonistic antibodyarthritisautoimmune inflammationcolitismonocyteneutrophilSIRPα

Identifiers

PMID37490914
PMCPMC10439247
OpenAlexW4385214261

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.