Evidence map›Paper›PMID 33253355›Full record

ArticleBrain : a journal of neurology2020

Brain cancer induces systemic immunosuppression through release of non-steroid soluble mediators.

Katayoun Ayasoufi, Christian K Pfaller, Laura Evgin, Roman H Khadka, Zachariah P Tritz, Emma N Goddery, Cori E Fain, Lila T Yokanovich, Benjamin T Himes, Fang Jin and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Brain : a journal of neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 5% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Immunotherapy for Glioma: A compartmental framework for resistance and rational combination design.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Oncolytic virus M1 reinvigorates CD8Cellular & molecular immunology · 2026
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Thymic regeneration and tumor immunotherapy.Frontiers in immunology · 2026
    Review
  19. Article
  20. Review

9 more citing papers are in PubMed but not listed here.

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

18 authors at 2 institutions in 2 countries.

Katayoun AyasoufiMayo Clinic Department of Immunology, Rochester, MN, USA.
Christian K PfallerMayo Clinic Department of Molecular Medicine, Rochester, MN, USA.
Laura EvginMayo Clinic Department of Molecular Medicine, Rochester, MN, USA.
Roman H KhadkaMayo Clinic Department of Immunology, Rochester, MN, USA.
Zachariah P TritzMayo Clinic Department of Immunology, Rochester, MN, USA.
Emma N GodderyMayo Clinic Department of Immunology, Rochester, MN, USA.
Cori E FainMayo Clinic Department of Immunology, Rochester, MN, USA.
Lila T YokanovichMayo Clinic Department of Immunology, Rochester, MN, USA.
Benjamin T HimesMayo Clinic Department of Immunology, Rochester, MN, USA.
Fang JinMayo Clinic Department of Immunology, Rochester, MN, USA.
Jiaying ZhengMayo Clinic Department of Molecular Medicine, Rochester, MN, USA.
Matthew R SchuelkeMayo Clinic Department of Immunology, Rochester, MN, USA.
Michael J HansenMayo Clinic Department of Immunology, Rochester, MN, USA.
Wesley TungMayo Clinic Department of Immunology, Rochester, MN, USA.
Ian F ParneyMayo Clinic Department of Immunology, Rochester, MN, USA.
Larry R PeaseMayo Clinic Department of Immunology, Rochester, MN, USA.
Richard G VileMayo Clinic Department of Immunology, Rochester, MN, USA.
Aaron J JohnsonMayo Clinic Department of Immunology, Rochester, MN, USA.
Mayo Clinic in Arizona · USMayo Clinic · US

Funding

CD8 T cell mediated disruption of Blood Brain Barrier Tight JunctionsR01NS103212 · NINDS · MAYO CLINIC ROCHESTER · PI Aaron J Johnson · 2017 to 2026
$4.6M
PHD TRAINING PROGRAM IN BASIC IMMUNOLOGYT32AI007425 · NIAID · MAYO CLINIC ROCHESTER · PI SHAPIRO, VIRGINIA SMITH · 1995 to 2020
$3.6M
Research Training Program in Neuro-OncologyT32CA217836 · NCI · MAYO CLINIC ROCHESTER · PI O'NEILL, BRIAN PATRICK, VILE, RICHARD G. · 2018 to 2022
$1.4M
Initiation of CD8 T cell-mediated BBB disruption and neuronal involvement in experimental cerebral malariaF31NS116924 · NINDS · MAYO CLINIC ROCHESTER · PI FAIN, CORI ELIZABETH · 2020 to 2021
$92k
NCI NIH HHS T32 CA217836NIAID NIH HHS T32 AI007425NINDS NIH HHS F31 NS116924NINDS NIH HHS R01 NS103212
6 · The paper itself

Abstract

Immunosuppression of unknown aetiology is a hallmark feature of glioblastoma and is characterized by decreased CD4 T-cell counts and downregulation of major histocompatibility complex class II expression on peripheral blood monocytes in patients. This immunosuppression is a critical barrier to the successful development of immunotherapies for glioblastoma. We recapitulated the immunosuppression observed in glioblastoma patients in the C57BL/6 mouse and investigated the aetiology of low CD4 T-cell counts. We determined that thymic involution was a hallmark feature of immunosuppression in three distinct models of brain cancer, including mice harbouring GL261 glioma, B16 melanoma, and in a spontaneous model of diffuse intrinsic pontine glioma. In addition to thymic involution, we determined that tumour growth in the brain induced significant splenic involution, reductions in peripheral T cells, reduced MHC II expression on blood leucocytes, and a modest increase in bone marrow resident CD4 T cells. Using parabiosis we report that thymic involution, declines in peripheral T-cell counts, and reduced major histocompatibility complex class II expression levels were mediated through circulating blood-derived factors. Conversely, T-cell sequestration in the bone marrow was not governed through circulating factors. Serum isolated from glioma-bearing mice potently inhibited proliferation and functions of T cells both in vitro and in vivo. Interestingly, the factor responsible for immunosuppression in serum is non-steroidal and of high molecular weight. Through further analysis of neurological disease models, we determined that the immunosuppression was not unique to cancer itself, but rather occurs in response to brain injury. Non-cancerous acute neurological insults also induced significant thymic involution and rendered serum immunosuppressive. Both thymic involution and serum-derived immunosuppression were reversible upon clearance of brain insults. These findings demonstrate that brain cancers cause multifaceted immunosuppression and pinpoint circulating factors as a target of intervention to restore immunity.

Indexed as

Immune ToleranceAnimalsBone Marrow CellsBrain NeoplasmsCD4-Positive T-LymphocytesCell ProliferationDisease ProgressionFemaleGenes, MHC Class IIGlioblastomaGliomaInflammation MediatorsMaleMelanoma, ExperimentalMiceMice, Inbred C57BLInflammation MediatorsglioblastomaimmunosuppressionneuroimmunologyT cellsthymus

Identifiers

PMID33253355
PMCPMC7954397
OpenAlexW3107657804

What OpenQuestion holds

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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.