Evidence map›Paper›PMID 34845863›Full record

ReviewJournal of diabetes investigation2022

Role of the adaptive immune system in diabetic kidney disease.

Lingyun Kong, Sofianos Andrikopoulos, Richard J MacIsaac, Laura K Mackay, David J Nikolic-Paterson, Niloufar Torkamani, Neda Zafari, Evelyn C S Marin, Elif I Ekinci

Abstract readReview
In one paragraph

Review in Journal of diabetes investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing 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

43 citing papers in PubMed.

  1. Trial
  2. Trial
  3. Article
  4. Review
  5. Inflammation and Diabetic Kidney Disease.International journal of molecular sciences · 2026
    Review
  6. Review
  7. Article
  8. Review
  9. Immunomodulatory Functions of Intercalated Cells in Kidney Autoimmunity.bioRxiv : the preprint server for biology · 2025
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Endothelin-1 signaling in the kidney: recent advances and remaining gaps.American journal of physiology. Renal physiology · 2025
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  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

9 authors.

Lingyun KongDepartment of Medicine, Austin Health, University of Melbourne, Melbourne, Victoria, Australia.
Sofianos AndrikopoulosDepartment of Medicine, Austin Health, University of Melbourne, Melbourne, Victoria, Australia.
Richard J MacIsaacDepartment of Medicine, Austin Health, University of Melbourne, Melbourne, Victoria, Australia.ORCID https://orcid.org/0000-0001-8058-6977
Laura K MackayDepartment of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, The University of Melbourne, Melbourne, Victoria, Australia.
David J Nikolic-PatersonDepartment of Nephrology, Monash Medical Center and Monash University Center for Inflammatory Diseases, Melbourne, Victoria, Australia.
Niloufar TorkamaniDepartment of Medicine, Austin Health, University of Melbourne, Melbourne, Victoria, Australia.
Neda ZafariDepartment of Medicine, Austin Health, University of Melbourne, Melbourne, Victoria, Australia.
Evelyn C S MarinCollege of Sport and Exercise Science, Victoria University, Melbourne, Victoria, Australia.
Elif I EkinciDepartment of Medicine, Austin Health, University of Melbourne, Melbourne, Victoria, Australia.ORCID https://orcid.org/0000-0003-2372-395X

Funding

China Scholarship Council 201806230303
6 · The paper itself

Abstract

Diabetic kidney disease (DKD) is a highly prevalent complication of diabetes and the leading cause of end-stage kidney disease. Inflammation is recognized as an important driver of progression of DKD. Activation of the immune response promotes a pro-inflammatory milieu and subsequently renal fibrosis, and a progressive loss of renal function. Although the role of the innate immune system in diabetic renal disease has been well characterized, the potential contribution of the adaptive immune system remains poorly defined. Emerging evidence in experimental models of DKD indicates an increase in the number of T cells in the circulation and in the kidney cortex, that in turn triggers secretion of inflammatory mediators such as interferon-γ and tumor necrosis factor-α, and activation of cells in innate immune response. In human studies, the number of T cells residing in the interstitial region of the kidney correlates with the degree of albuminuria in people with type 2 diabetes. Here, we review the role of the adaptive immune system, and associated cytokines, in the development of DKD. Furthermore, the potential therapeutic benefits of targeting the adaptive immune system as a means of preventing the progression of DKD are discussed.

Indexed as

Diabetes Mellitus, Type 2Diabetic NephropathiesAlbuminuriaHumansImmune SystemKidneyAdaptive immune systemDiabetic kidney diseaseInflammation

Identifiers

PMID34845863
PMCPMC8847140

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.