ReviewSpringer seminars in immunopathology1999
Natural and induced regulation of Th1/Th2 balance.
Review in Springer seminars in immunopathology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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
7 citing papers in PubMed, 19 citations in OpenAlex.
- Functional and phenotypic characterization of peripheral blood mononuclear cells from tuberculosis patients in Southern Thailand.Frontiers in immunology · 2025Article
- Allelic combinations of promoter and exon 2 in DQB1 in dogs and wolves.Journal of molecular evolution · 2008Article
- Article
- Enhanced tolerance to autoimmune uveitis in CD200-deficient mice correlates with a pronounced Th2 switch in response to antigen challenge.Journal of immunology (Baltimore, Md. : 1950) · 2005Article
- Patterned variation in murine MHC promoters.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Polymorphism in regulatory gene sequences.Genome biology · 2001Article
- CC chemokine receptor (CCR)2 is required for langerhans cell migration and localization of T helper cell type 1 (Th1)-inducing dendritic cells. Absence of CCR2 shifts the Leishmania major-resistant phenotype to a susceptible state dominated by Th2 cytokines, b cell outgrowth, and sustained neutrophilic inflammation.The Journal of experimental medicine · 2000Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Because Th1/Th2 balance is perturbed during immunological disease, the design of strategies aiming at its rectification has become a priority. The alteration of the balance in pregnancy so as to promote survival of the fetal allograft lends credibility to this aim. Attenuation of the activation signal delivered through the T cell receptor (TCR) represents a promising approach. It is supported by the high level of polymorphism in the MHC class II promoter, which regulates the natural TCR signal and thus modulates Th1/Th2 differentiation. Further support comes from the Th2 shift that occurs in JNK knockout mice, and with kinase inhibitors and anti-CD4 monoclonal antibodies applied in vitro. The approach has implications for nasal tolerance and inhibition of IL-12 production. The further range of options for Th1/Th2 modulation, which are presented throughout this issue of the journal, are here summarised and evaluated.
Indexed as
Identifiers
What OpenQuestion holds
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.