Evidence map›Paper›PMID 27109641›Full record

ReviewClinical immunology (Orlando, Fla.)2017

T cells and IL-17 in lupus nephritis.

Tomohiro Koga, Kunihiro Ichinose, George C Tsokos

Open access · greenAbstract readReview
In one paragraph

Review in Clinical immunology (Orlando, Fla.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
11.1field-weighted citation impact, top 1% 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

61 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
  2. Review
  3. Can we cure autoimmunity?Current opinion in immunology · 2026
    Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. The IL-17 family in diseases: from bench to bedside.Signal transduction and targeted therapy · 2023
    Review
  17. Review
  18. Article
  19. Review
  20. Article

1 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

3 authors at 2 institutions in 2 countries.

Tomohiro KogaDivision of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA; Department of Immunology and Rheumatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan. Electronic address: tkoga@nagasaki-u.ac.jp.
Kunihiro IchinoseDivision of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA; Department of Immunology and Rheumatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
George C TsokosDivision of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Electronic address: gtsokos@bidmc.harvard.edu.
Harvard University · USNagasaki University · JP

Funding

Targeting CaMK4 in SLER01AR064350 · NIAMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TSOKOS, GEORGE C · 2013 to 2017
$1.8M
NIAMS NIH HHS R01 AR064350
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a complicated autoimmune disorder characterized by autoantibodies production, immune complex formation, and immune dysregulation, resulting in damage of multiple organs including the kidney. Lupus nephritis (LN) is the most common severe manifestation of SLE involving the majority of patients. Even though there are a number of reports indicating that interleukin-17 (IL-17) and Th17 cells play important roles in the pathogenesis of LN, the precise molecular mechanisms underline the development of LN have not been totally elucidated. In this review, we briefly summarize general characteristics of T and IL-17 cells in SLE. In addition, we discuss in detail T cell signaling pathways which control IL-17 production in patients with LN and in glomerulonephritis in lupus-prone mice. A better understanding of signaling and gene regulation defects in LN will lead to the identification of novel therapeutic targets and predictive biomarkers for diagnosis and prognosis of this disease.

Indexed as

AnimalsHumansInterleukin-17Lupus NephritisT-LymphocytesInterleukin-17Interleukin-17Lupus nephritisSystemic lupus erythematosusT cells

Identifiers

PMID27109641
PMCPMC5074925
OpenAlexW2343203956

What OpenQuestion holds

Textmetadata
LicenceTDM
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.