Evidence map›Paper›PMID 28635960›Full record

ArticleNature communications2017

Somatic mutations in clonally expanded cytotoxic T lymphocytes in patients with newly diagnosed rheumatoid arthritis.

P Savola, T Kelkka, H L Rajala, A Kuuliala, K Kuuliala, S Eldfors, P Ellonen, S Lagström, M Lepistö, T Hannunen and 9 more

Abstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing 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

69 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Unmet needs in autoimmune liver diseases.Current opinion in immunology · 2025
    Review
  9. Review
  10. Mitochondrial response to fever boosts TImmunometabolism (Cobham, Surrey) · 2025
    Article
  11. Article
  12. Article
  13. DOGMA-seq and multimodal, single-cell analysis in acute myeloid leukemia.International review of cell and molecular biology · 2025
    Review
  14. Article
  15. Article
  16. Large granular lymphocyte leukemia: a clonal disorder with autoimmune manifestations.Hematology. American Society of Hematology. Education Program · 2024
    Review
  17. Review
  18. Article
  19. Genetic variation across and within individuals.Nature reviews. Genetics · 2024
    Review
  20. Article

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

19 authors.

P SavolaHematology Research Unit Helsinki, University of Helsinki and Department of Hematology, Helsinki University Hospital Comprehensive Cancer Centre, Haartmaninkatu 8, FIN-00290 Helsinki, Finland.
T KelkkaHematology Research Unit Helsinki, University of Helsinki and Department of Hematology, Helsinki University Hospital Comprehensive Cancer Centre, Haartmaninkatu 8, FIN-00290 Helsinki, Finland.ORCID 0000-0003-1085-6382
H L RajalaHematology Research Unit Helsinki, University of Helsinki and Department of Hematology, Helsinki University Hospital Comprehensive Cancer Centre, Haartmaninkatu 8, FIN-00290 Helsinki, Finland.
A KuulialaBacteriology and Immunology, Medicum, University of Helsinki, Haartmaninkatu 3, FIN-00290 Helsinki, Finland.
K KuulialaBacteriology and Immunology, Medicum, University of Helsinki, Haartmaninkatu 3, FIN-00290 Helsinki, Finland.
S EldforsInstitute for Molecular Medicine Finland (FIMM), University of Helsinki, Tukholmankatu 8, FIN-00290 Helsinki, Finland.
P EllonenInstitute for Molecular Medicine Finland (FIMM), University of Helsinki, Tukholmankatu 8, FIN-00290 Helsinki, Finland.
S LagströmInstitute for Molecular Medicine Finland (FIMM), University of Helsinki, Tukholmankatu 8, FIN-00290 Helsinki, Finland.
M LepistöInstitute for Molecular Medicine Finland (FIMM), University of Helsinki, Tukholmankatu 8, FIN-00290 Helsinki, Finland.
T HannunenInstitute for Molecular Medicine Finland (FIMM), University of Helsinki, Tukholmankatu 8, FIN-00290 Helsinki, Finland.
E I AnderssonHematology Research Unit Helsinki, University of Helsinki and Department of Hematology, Helsinki University Hospital Comprehensive Cancer Centre, Haartmaninkatu 8, FIN-00290 Helsinki, Finland.
R K KhajuriaHematology Research Unit Helsinki, University of Helsinki and Department of Hematology, Helsinki University Hospital Comprehensive Cancer Centre, Haartmaninkatu 8, FIN-00290 Helsinki, Finland.
T JaatinenHistocompatibility Testing Laboratory, Finnish Red Cross Blood Service, Kivihaantie 7, FIN-00310 Helsinki, Finland.
R KoivuniemiDepartment of Rheumatology, University of Helsinki and Helsinki University Hospital, Haartmaninkatu 4, FIN-00290 Helsinki, Finland.
H RepoBacteriology and Immunology, Medicum, University of Helsinki, Haartmaninkatu 3, FIN-00290 Helsinki, Finland.
J SaarelaInstitute for Molecular Medicine Finland (FIMM), University of Helsinki, Tukholmankatu 8, FIN-00290 Helsinki, Finland.
K PorkkaHematology Research Unit Helsinki, University of Helsinki and Department of Hematology, Helsinki University Hospital Comprehensive Cancer Centre, Haartmaninkatu 8, FIN-00290 Helsinki, Finland.
M Leirisalo-RepoDepartment of Rheumatology, University of Helsinki and Helsinki University Hospital, Haartmaninkatu 4, FIN-00290 Helsinki, Finland.
S MustjokiHematology Research Unit Helsinki, University of Helsinki and Department of Hematology, Helsinki University Hospital Comprehensive Cancer Centre, Haartmaninkatu 8, FIN-00290 Helsinki, Finland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Somatic mutations contribute to tumorigenesis. Although these mutations occur in all proliferating cells, their accumulation under non-malignant conditions, such as in autoimmune disorders, has not been investigated. Here, we show that patients with newly diagnosed rheumatoid arthritis have expanded CD8+ T-cell clones; in 20% (5/25) of patients CD8+ T cells, but not CD4+ T cells, harbour somatic mutations. In healthy controls (n=20), only one mutation is identified in the CD8+ T-cell pool. Mutations exist exclusively in the expanded CD8+ effector-memory subset, persist during follow-up, and are predicted to change protein functions. Some of the mutated genes (SLAMF6, IRF1) have previously been associated with autoimmunity. RNA sequencing of mutation-harbouring cells shows signatures corresponding to cell proliferation. Our data provide evidence of accumulation of somatic mutations in expanded CD8+ T cells, which may have pathogenic significance for RA and other autoimmune diseases.

Indexed as

MutationAdultAgedAge FactorsArthritis, RheumatoidCase-Control StudiesCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesFemaleGenes, T-Cell Receptor betaHigh-Throughput Nucleotide SequencingHumansInterferon Regulatory Factor-1MaleMiddle AgedProspective StudiesInterferon Regulatory Factor-1IRF1 protein, humanSignaling Lymphocytic Activation Molecule FamilySLAMF6 protein, human

Identifiers

PMID28635960
PMCPMC5482061

What Socratic holds

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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 Socratic graph.