Evidence map›Paper›PMID 42427724›Full record

ArticlebioRxiv : the preprint server for biology2026

CD38 defines a therapeutically targetable pathogenic T cell population for precision immunotherapy in autoimmune diabetes.

Shiva Pathak, Rizwan Ahmed, Nadine Nagy, Sooyeon Lee, Cameron S Bader, Shobha Regmi, Bettina P Iliopoulou, Pin-I Chen, Biki Gupta, Alejandro Villar-Prados and 10 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for 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.

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

20 authors.

Shiva PathakDivision of Blood and Marrow Transplantation and Cellular Therapy, Stanford University School of Medicine; Stanford, CA, USA.ORCID 0000-0003-1275-8516
Rizwan AhmedDepartment of Immunology and Rheumatology, Stanford University School of Medicine; Stanford, CA, USA.
Nadine NagyDivision of Blood and Marrow Transplantation and Cellular Therapy, Stanford University School of Medicine; Stanford, CA, USA.
Sooyeon LeeStanford Diabetes Research Center, Stanford University School of Medicine; Stanford, CA, USA.
Cameron S BaderDivision of Blood and Marrow Transplantation and Cellular Therapy, Stanford University School of Medicine; Stanford, CA, USA.
Shobha RegmiDepartment of Pediatric Gastroenterology, Stanford University School of Medicine; Stanford, CA, USA.
Bettina P IliopoulouDivision of Blood and Marrow Transplantation and Cellular Therapy, Stanford University School of Medicine; Stanford, CA, USA.
Pin-I ChenDivision of Blood and Marrow Transplantation and Cellular Therapy, Stanford University School of Medicine; Stanford, CA, USA.
Biki GuptaDivision of Blood and Marrow Transplantation and Cellular Therapy, Stanford University School of Medicine; Stanford, CA, USA.
Alejandro Villar-PradosDivision of Blood and Marrow Transplantation and Cellular Therapy, Stanford University School of Medicine; Stanford, CA, USA.
Yong Bin KimDivision of Blood and Marrow Transplantation and Cellular Therapy, Stanford University School of Medicine; Stanford, CA, USA.
Noor HusseinDivision of Blood and Marrow Transplantation and Cellular Therapy, Stanford University School of Medicine; Stanford, CA, USA.
Emily SooHooDivision of Blood and Marrow Transplantation and Cellular Therapy, Stanford University School of Medicine; Stanford, CA, USA.
Abigail TwoyDivision of Blood and Marrow Transplantation and Cellular Therapy, Stanford University School of Medicine; Stanford, CA, USA.
Avnesh S ThakorDepartment of Radiology, Stanford University School of Medicine; Stanford, CA, USA.
Kent P JensenDivision of Blood and Marrow Transplantation and Cellular Therapy, Stanford University School of Medicine; Stanford, CA, USA.
Paul J UtzDepartment of Immunology and Rheumatology, Stanford University School of Medicine; Stanford, CA, USA.
Mark M DavisDepartment of Microbiology and Immunology, Stanford University School of Medicine; Stanford, CA, USA.
Justin P AnnesDivision of Endocrinology, Stanford University School of Medicine; Stanford, CA, USA.ORCID 0000-0001-8431-3589
Everett H MeyerDivision of Blood and Marrow Transplantation and Cellular Therapy, Stanford University School of Medicine; Stanford, CA, USA.

Funding

Stanford Islet Research CoreP30DK116074 · NIDDK · STANFORD UNIVERSITY · PI Seung K Kim · 2017 to 2026
$19.5M
Diabetes, Endocrinology and Metabolism Training GrantT32DK007217 · NIDDK · STANFORD UNIVERSITY · PI Justin Pierce Annes, David Matthew Maahs · 1987 to 2026
$7.2M
Engineered Immune Cells for T1DR01DK132549 · NIDDK · STANFORD UNIVERSITY · PI MEYER, EVERETT · 2022 to 2025
$3.1M
A stem cell activated cryogel bioscaffold that restores islet bioenergetics while providing oxygen and nutrients at extravascular sites of transplantationR01DK129343 · NIDDK · STANFORD UNIVERSITY · PI Avnesh Sinh Thakor · 2022 to 2026
$2.8M
Facilitating islet implantation and engraftment following transplantation using primed umbilical cord mesenchymal stem therapies and focused ultrasoundR01DK141802 · NIDDK · STANFORD UNIVERSITY · PI Avnesh Sinh Thakor · 2025 to 2026
$1.5M
NIDDK NIH HHS P30 DK116074NIDDK NIH HHS R01 DK129343NIDDK NIH HHS R01 DK132549NIDDK NIH HHS R01 DK141802NIDDK NIH HHS T32 DK007217
6 · The paper itself

Abstract

Type 1 diabetes (T1D) is caused by T cell-mediated autoimmune destruction of insulin-producing islet β-cells. Treatment with T-cell depleting therapies delays the progression of stage 2 and 3 T1D, but these agents exert broad immunosuppressive effects on T cell populations, including T regulatory cells (Tregs), which are key in promoting immune tolerance. We evaluated non-obese diabetic (NOD) mice and recently diagnosed T1D patients and identified CD38 as a marker for pathogenic T cell populations. Using adoptive T-cell transfer in Recombination Activating Gene 1 knockout NOD mice and in a humanized mouse model of autoimmune diabetes, we demonstrated that CD38-expressing autoreactive T cells drive diabetes pathogenesis. Furthermore, we found that selective depletion of CD38

Indexed as

Anti-CD38 mAbAutoreactive T cellsImmune toleranceT regulatory cellsType 1 diabetes

Identifiers

PMID42427724
PMCPMC13345075

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.