ArticleInfection and immunity2006
Neutralization or absence of the interleukin-23 pathway does not compromise immunity to mycobacterial infection.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 72 citations in OpenAlex.
- Rethinking TYK2 P1104A: a flawed evolutionary trade-off in tuberculosis?Frontiers in immunology · 2026Review
- Furamidine enhances IL-23-mediated autophagic response through IL-23R-TYK2-STAT3-dependent regulation of intracellular Ca²⁺ level to facilitate mycobacterial clearance in human macrophages.Medical microbiology and immunology · 2025Article
- Positioning Guselkumab in The Treatment Algorithm of Patients with Crohn's Disease.Biologics : targets & therapy · 2025Review
- Treatment of Psoriasis Patients with Latent Tuberculosis Using IL-17 and IL-23 Inhibitors: A Retrospective, Multinational, Multicentre Study.American journal of clinical dermatology · 2024Observational
- The Role of IL-23 Inhibitors in Crohn's Disease.Journal of clinical medicine · 2023Review
- Review
- Crossing the boundaries: IL-23 and its role in linking inflammation of the skin, gut and joints.Rheumatology (Oxford, England) · 2021Article
- Advancing Adjuvants forFrontiers in immunology · 2021Review
- Considerations for safety in the use of systemic medications for psoriasis and atopic dermatitis during the COVID-19 pandemic.Dermatologic therapy · 2020Review
- Tuberculosis and targeted synthetic or biologic DMARDs, beyond tumor necrosis factor inhibitors.Therapeutic advances in musculoskeletal disease · 2020Review
- Review
- Species-Specific Structural Requirements of Alpha-Branched Trehalose Diester Mincle Agonists.Frontiers in immunology · 2019Article
- The complex alteration in the network of IL-17-type cytokines in patients with hereditary angioedema.Clinical and experimental medicine · 2018Article
- Inhibition of IL-17A by secukinumab shows no evidence of increasedClinical & translational immunology · 2017Article
- Controlled Mycobacterium tuberculosis infection in mice under treatment with anti-IL-17A or IL-17F antibodies, in contrast to TNFα neutralization.Scientific reports · 2016Article
- CCR2 defines in vivo development and homing of IL-23-driven GM-CSF-producing Th17 cells.Nature communications · 2015Article
- The IL-23-IL-17 immune axis: from mechanisms to therapeutic testing.Nature reviews. Immunology · 2014Review
- Cytokine-based therapy in psoriasis.Clinical reviews in allergy & immunology · 2013Review
- IL-23 Contributes to Control of Chronic Helicobacter Pylori Infection and the Development of T Helper Responses in a Mouse Model.Frontiers in immunology · 2012Article
- Molecular immunity to mycobacteria: knowledge from the mutation and phenotype spectrum analysis of Mendelian susceptibility to mycobacterial diseases.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-23 (IL-23), a member of the IL-12 family, is a heterodimeric cytokine that is composed of the p40 subunit of IL-12 plus a unique p19 subunit. IL-23 is critical for autoimmune inflammation, in part due to its stimulation of the proinflammatory cytokine IL-17A. It is less clear, however, if IL-23 is required during the immune response to pathogens. We examined the role of IL-23 during Mycobacterium bovis BCG infection. We found that IL-23 reduces the bacterial burden and promotes granuloma formation when IL-12 is absent. However, IL-23 does not contribute substantially to host resistance when IL-12 is present, as the ability to control bacterial growth and form granulomata is not affected in IL-23p19-deficient mice and mice treated with a specific anti-IL-23p19 antibody. IL-23p19-deficient mice are also able to mount an effective memory response to secondary infection with BCG. While IL-23p19-deficient mice do not produce IL-17A, this cytokine is not necessary for effective control of infection, and antibody blocking of IL-17A in both wild-type and IL-12-deficient mice also has little effect on the bacterial burden. These data suggest that IL-23 by itself does not play an essential role in the protective immune response to BCG infection; however, the presence of IL-23 can partially compensate for the absence of IL-12. Furthermore, neutralization of IL-23 or IL-17A does not increase susceptibility to mycobacterial BCG infection.
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.