ArticlePloS one2013
IL-22 is mainly produced by IFNγ-secreting cells but is dispensable for host protection against Mycobacterium tuberculosis infection.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 43 citations in OpenAlex.
- CD4+ T cell cytokine responses to the DAR-901 booster vaccine in BCG-primed adults: A randomized, placebo-controlled trial.PloS one · 2019Trial
- Lineage-Dependent IFN-γ Responses to Drug-Sensitive and Isoniazid-ResistantInfection and drug resistance · 2026Article
- The evolving landscape of IL-10, IL-22 and IL-26 in pleurisy especially in tuberculous pleurisy.Respiratory research · 2024Review
- Helper T cell bias following tuberculosis chemotherapy identifies opportunities for therapeutic vaccination to prevent relapse.NPJ vaccines · 2023Article
- Current Knowledge of Th22 Cell and IL-22 Functions in Infectious Diseases.Pathogens (Basel, Switzerland) · 2023Review
- High-DoseCells · 2022Article
- Characterization ofJournal of immunology (Baltimore, Md. : 1950) · 2022Article
- Tuberculostearic Acid-Containing Phosphatidylinositols as Markers of Bacterial Burden in Tuberculosis.ACS infectious diseases · 2022Article
- Th22 Cells Are a Major Contributor to the Mycobacterial CD4Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Article
- Immune defects in patients with pulmonaryERJ open research · 2020Article
- Circulating HLA-DR+CD4+ effector memory T cells resistant to CCR5 and PD-L1 mediated suppression compromise regulatory T cell function in tuberculosis.PLoS pathogens · 2018Article
- Regulation of T helper cell responses during antigen presentation by norepinephrine-exposed endothelial cells.Immunology · 2018Article
- IL-22: An Underestimated Player in Natural Resistance to Tuberculosis?Frontiers in immunology · 2018Review
- Cancer cells induce interleukin-22 production from memory CD4Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Novel role for IL-22 in protection during chronic Mycobacterium tuberculosis HN878 infection.Mucosal immunology · 2017Article
- T-bet over-expression regulates aryl hydrocarbon receptor-mediated T helper type 17 differentiation through an interferon (IFN)γ-independent pathway.Clinical and experimental 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
- Cytokines and Chemokines in Mycobacterium tuberculosis Infection.Microbiology spectrum · 2016Review
- Pathogenic T helper type 17 cells contribute to type 1 diabetes independently of interleukin-22.Clinical and experimental immunology · 2016Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anti-inflammatory treatment of autoimmune diseases is associated with an increased risk of reactivation tuberculosis (TB). Besides interleukin (IL-17)A, IL-22 represents a classical T helper (TH)17 cytokine and shares similar pathological effects in inflammatory diseases such as psoriasis or arthritis. Whereas IL-17A supports protective immune responses during mycobacterial infections, the role of IL-22 after infection with Mycobacterium tuberculosis (Mtb) is yet poorly characterized. Therefore, we here characterize the cell types producing IL-22 and the protective function of this cytokine during experimental TB in mice. Like IL-17A, IL-22 is expressed early after infection with Mtb in an IL-23-dependent manner. Surprisingly, the majority of IL-22-producing cells are not positive for IL-17A but have rather functional characteristics of interferon-gamma-producing TH1 cells. Although we found minor differences in the number of naive and central memory T cells as well as in the frequency of TH1 and polyfunctional T cells in mice deficient for IL-22, the absence of IL-22 does not affect the outcome of Mtb infection. Our study revealed that although produced by TH1 cells, IL-22 is dispensable for protective immune responses during TB. Therefore, targeting of IL-22 in inflammatory disease may represent a therapeutic approach that does not incur the danger of reactivation TB.
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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.