Evidence map›Paper›PMID 26036802›Full record

ArticleBlood2015

CD8+ T cells are predominantly protective and required for effective steroid therapy in murine models of immune thrombocytopenia.

Li Ma, Elisa Simpson, June Li, Min Xuan, Miao Xu, Laura Baker, Yan Shi, Issaka Yougbaré, Xiaozhong Wang, Guangheng Zhu and 5 more

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

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Correlation between the CD8Frontiers in pediatrics · 2026
    Article
  6. Article
  7. Natural killer cell granule protein 7 contributes to CD8Research and practice in thrombosis and haemostasis · 2025
    Article
  8. Article
  9. Review
  10. Review
  11. Novel Biomarkers for Diagnosis and Monitoring of Immune Thrombocytopenia.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

15 authors at 5 institutions in 2 countries.

Li MaToronto Platelet Immunobiology Group, Toronto, ON, Canada; Department of Laboratory Medicine, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, ON, Canada; Canadian Blood Services, Toronto, ON, Canada;
Elisa SimpsonToronto Platelet Immunobiology Group, Toronto, ON, Canada; Department of Laboratory Medicine, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, ON, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada;
June LiToronto Platelet Immunobiology Group, Toronto, ON, Canada; Department of Laboratory Medicine, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, ON, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada;
Min XuanToronto Platelet Immunobiology Group, Toronto, ON, Canada; Department of Laboratory Medicine, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, ON, Canada; State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China;
Miao XuToronto Platelet Immunobiology Group, Toronto, ON, Canada; Department of Laboratory Medicine, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, ON, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada;
Laura BakerToronto Platelet Immunobiology Group, Toronto, ON, Canada; Department of Laboratory Medicine, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, ON, Canada; Canadian Blood Services, Toronto, ON, Canada;
Yan ShiToronto Platelet Immunobiology Group, Toronto, ON, Canada; Department of Laboratory Medicine, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, ON, Canada; Department of Haematology, Qilu Hospital, Shandong University, Jinan, China;
Issaka YougbaréToronto Platelet Immunobiology Group, Toronto, ON, Canada; Department of Laboratory Medicine, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, ON, Canada; Canadian Blood Services, Toronto, ON, Canada;
Xiaozhong WangToronto Platelet Immunobiology Group, Toronto, ON, Canada; Department of Laboratory Medicine, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, ON, Canada; The Second Affiliated Hospital of Nanchang University, Jiangxi, China; and.
Guangheng ZhuToronto Platelet Immunobiology Group, Toronto, ON, Canada; Department of Laboratory Medicine, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, ON, Canada;
Pingguo ChenToronto Platelet Immunobiology Group, Toronto, ON, Canada; Department of Laboratory Medicine, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, ON, Canada; Canadian Blood Services, Toronto, ON, Canada;
Gerald J Prud'hommeDepartment of Laboratory Medicine, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, ON, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada;
Alan H LazarusToronto Platelet Immunobiology Group, Toronto, ON, Canada; Department of Laboratory Medicine, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, ON, Canada; Canadian Blood Services, Toronto, ON, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada; Department of Medicine and.
John FreedmanToronto Platelet Immunobiology Group, Toronto, ON, Canada; Department of Laboratory Medicine, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, ON, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada; Department of Medicine and.
Heyu NiToronto Platelet Immunobiology Group, Toronto, ON, Canada; Department of Laboratory Medicine, Keenan Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, ON, Canada; Canadian Blood Services, Toronto, ON, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada; Department of Medicine and Department of Physiology, University of Toronto, ON, Canada.
St. Michael's Hospital · CAUniversity of Toronto · CACanadian Blood Services · CAInstitute of Hematology & Blood Diseases Hospital · CNQilu Hospital of Shandong University · CN

Funding

Canadian Institutes of Health Research MOP 97918
6 · The paper itself

Abstract

Immune thrombocytopenia (ITP) is a common autoimmune bleeding disorder characterized by autoantibodies targeting platelet surface proteins, most commonly GPIIbIIIa (αIIbβ3 integrin), leading to platelet destruction. Recently, CD8(+) cytotoxic T-lymphocytes (CTLs) targeting platelets and megakaryocytes have also been implicated in thrombocytopenia. Because steroids are the most commonly administered therapy for ITP worldwide, we established both active (immunized splenocyte engraftment) and passive (antibody injection) murine models of steroid treatment. Surprisingly, we found that, in both models, CD8(+) T cells limited the severity of the thrombocytopenia and were required for an efficacious response to steroid therapy. Conversely, CD8(+) T-cell depletion led to more severe thrombocytopenia, whereas CD8(+) T-cell transfusion ameliorated thrombocytopenia. CD8(+) T-regulatory cell (Treg) subsets were detected, and interestingly, dexamethasone (DEX) treatment selectively expanded CD8(+) Tregs while decreasing CTLs. In vitro coculture studies revealed CD8(+) Tregs suppressed CD4(+) and CD19(+) proliferation, platelet-associated immunoglobulin G generation, CTL cytotoxicity, platelet apoptosis, and clearance. Furthermore, we found increased production of anti-inflammatory interleukin-10 in coculture studies and in vivo after steroid treatment. Thus, we uncovered subsets of CD8(+) Tregs and demonstrated their potent immunosuppressive and protective roles in experimentally induced thrombocytopenia. The data further elucidate mechanisms of steroid treatment and suggest therapeutic potential for CD8(+) Tregs in immune thrombocytopenia.

Indexed as

AnimalsBlood PlateletsCD8-Positive T-LymphocytesCombined Modality TherapyDexamethasoneDisease Models, AnimalImmunotherapy, AdoptiveLymphocyte DepletionMiceMice, Inbred BALB CMice, KnockoutPlatelet Glycoprotein GPIIb-IIIa ComplexPurpura, Thrombocytopenic, IdiopathicT-Lymphocytes, CytotoxicTreatment OutcomeDexamethasonePlatelet Glycoprotein GPIIb-IIIa Complex

Identifiers

PMID26036802
PMCPMC4505012
OpenAlexW1606013393

What OpenQuestion holds

Textmetadata
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.