ReviewAnnals of the New York Academy of Sciences2010
Th1 and Th17 cells: adversaries and collaborators.
Review in Annals of the New York Academy of Sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 208 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
208 citing papers in PubMed, 403 citations in OpenAlex.
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- Prevalence, outcomes, and predictive factors: a systematic literature review to inform the development of EULAR Points to Consider for the definition of Difficult-to-Manage and Treatment-Refractory psoriatic arthritis.EULAR rheumatology open · 2026Article
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- Gut microbial interaction networks control autoimmunity to neuroretina.Research square · 2026Article
- Sex matters: mechanistic insights into sex-driven patterns of autoimmunity and implications for pharmacotherapy.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Untangling the Complexity of Childhood Atopic Dermatitis: Phenotypes and Endotypes.Clinical reviews in allergy & immunology · 2026Review
- Effects of immune checkpoint inhibitors on the pulmonary circulation in lung cancer patients.International journal of cancer · 2026Article
- Circulating Fibrocytes: Cellular Mediators of Tissue Fibrosis.International journal of molecular sciences · 2026Review
- CCR2Discovery immunology · 2026Article
- Immunopathogenesis of severe pneumonia in children with emphasis on CD4+ T cells, Tim-3 and cytokine-mediated immune dysregulation.Frontiers in medicine · 2026Review
- Gut microbial interaction networks control autoimmunity to neuroretina.bioRxiv : the preprint server for biology · 2025Article
- Multiple sclerosis pathophysiology: a comprehensive review of genetic, environmental, and immunological drivers.Inflammopharmacology · 2025Review
- Notch3 destabilizes regulatory T cells to drive autoimmune neuroinflammation in multiple sclerosis.Immunity · 2025Article
- Immunization with Complete Freund's Adjuvant Reveals Trained Immunity-like Features in A/J Mice.Vaccines · 2025Article
- The NLRP3 inflammasome pathway contributes to chronic inflammation in experimental autoimmune uveitis.Animal models and experimental medicine · 2025Article
- Relationship Between Obesity and Depression Considering the Inflammatory Theory.International journal of molecular sciences · 2025Review
- Shared genetic association between inflammatory bowel disease and acute myeloid leukemia: insights from mendelian randomization and transcriptomic analyses.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Strategies and limitations of the bat immune response toFrontiers in immunology · 2025Review
- Immunological mechanisms in Meniere's disease.Frontiers in immunology · 2025Review
148 more citing papers are in PubMed but not listed here.
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 2 institutions in 1 country.
Funding
Abstract
Autoreactive effector CD4+ T cells have been associated with the pathogenesis of autoimmune disorders. Early studies implicated the interferon (IFN)-gamma-producing T helper (Th)1 subset of CD4+ cells as the causal agents in the pathogenesis of autoimmunity. However, further studies have suggested a more complex story. In models thought to be driven by Th1 cells, mice lacking the hallmark Th1 cytokine IFN-gamma were not protected but tended to have enhanced susceptibility to disease. Identification of the IL-17-producing CD4+ effector cell lineage (Th17) has helped shed light on this issue. Th17 effector cells are induced in parallel to Th1, and, like Th1, polarized Th17 cells have the capacity to cause inflammation and autoimmune disease. This, together with the finding that deficiency of the Th17-related cytokine IL-23 but not the Th1-related cytokine IL-12 causes resistance, led to the notion that Th17 cells are the chief contributors to autoimmune tissue inflammation. Nevertheless, mice lacking IL-17 are not protected from disease and display elevated numbers of IFN-gamma-producing CD4+ T cells, and, in some cases, lack of IFN-gamma does confer resistance. Recent studies report overlapping as well as differential roles of these cells in tissue inflammation, which suggests the existence of a more complex relationship between these two effector T-cell subsets than has hitherto been suspected. This review will attempt to bring together current information regarding interaction, balance, and collaborative potential between the Th1 and Th17 effector lineages.
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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.