ReviewClinical and experimental immunology2005
Glomerulonephritis, Th1 and Th2: what's new?
Review in Clinical and experimental immunology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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.
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.
Who cites it
31 citing papers in PubMed, 83 citations in OpenAlex.
- Immune cell crosstalk between ANCA-associated vasculitis and IgG4-related disease: an unresolved pathogenic link.Frontiers in immunology · 2025Review
- Metalloporphyrins as Tools for Deciphering the Role of Heme Oxygenase in Renal Immune Injury.International journal of molecular sciences · 2023Review
- T cells and their products in diabetic kidney disease.Frontiers in immunology · 2023Review
- Identification of Unique Genetic Biomarkers of Various Subtypes of Glomerulonephritis Using Machine Learning and Deep Learning.Biomolecules · 2022Article
- Phospholipase A2 receptor is associated with hypercoagulable status in membranous nephropathy: a narrative review.Annals of translational medicine · 2022Review
- Assessing the Global Impact on the Mouse Kidney After Traumatic Brain Injury: A Transcriptomic Study.Journal of inflammation research · 2022Article
- Canagliflozin reverses Th1/Th2 imbalance and promotes podocyte autophagy in rats with membranous nephropathy.Frontiers in immunology · 2022Article
- Low serum IgG4 level: a potential diagnostic biomarker for IgA nephropathy.Annals of translational medicine · 2021Article
- Myeloid-Derived Suppressor Cells Promote the Progression of Primary Membranous Nephropathy by Enhancing Th17 Response.Frontiers in immunology · 2020Article
- Clinicopathological analysis of ANCA-associated glomerulonephritis focusing on plasma cell infiltrate.Clinical and experimental nephrology · 2019Article
- MicroRNA-155-induced T lymphocyte subgroup drifting in IgA nephropathy.International urology and nephrology · 2017Article
- Article
- Studying cytokines of T helper cells in the kidney disease of IgA vasculitis (Henoch-Schönlein purpura).Pediatric nephrology (Berlin, Germany) · 2015Article
- Antiphospholipase A2 Receptor Autoantibodies: A Step Forward in the Management of Primary Membranous Nephropathy.BioMed research international · 2015Review
- Lutheran/basal cell adhesion molecule accelerates progression of crescentic glomerulonephritis in mice.Kidney international · 2014Article
- Expression of Ser729 phosphorylated PKCepsilon in experimental crescentic glomerulonephritis: an immunohistochemical study.European journal of histochemistry : EJH · 2014Article
- Differential diagnosis of lupus and primary membranous nephropathies by IgG subclass analysis.Clinical journal of the American Society of Nephrology : CJASN · 2012Article
- Pathogenesis of membranous nephropathy: recent advances and future challenges.Nature reviews. Nephrology · 2012Review
- Pathogenic role of effector cells and immunoglobulins in cationic bovine serum albumin-induced membranous nephropathy.Journal of clinical immunology · 2012Article
- Ferulic Acid, an Angelica sinensis-Derived Polyphenol, Slows the Progression of Membranous Nephropathy in a Mouse Model.Evidence-based complementary and alternative medicine : eCAM · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glomerulonephritis (GN), the major worldwide cause of chronic renal disease and renal failure, shows a wide spectrum of histological patterns, severity of injury and clinical outcomes that may be related to the nature of the nephritogenic immune response. In the majority of cases, there is evidence of a central role for cognate immunity in the initiation of human GN and contributions of both humoral and cellular effector mechanisms have been demonstrated in both humans and in animal models. T helper cell subsets are known to activate different immune effector mechanisms which influence disease outcomes in infectious and autoimmune diseases and evidence is now accumulating that Th1 and Th2 subsets direct diverging effector pathways that lead to different patterns and severity of glomerular injury in GN. Th1-predominant responses appear to be associated strongly with proliferative and crescentic forms of GN that result in severe renal injury, while Th2 responses are associated with membranous patterns of injury. The challenge remains to understand fully the relevance of T helper cell subset responses to the spectrum of human GN and to apply this new knowledge to the development of more potent and selective therapeutic strategies.
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Registered trials
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.