ArticleFrontiers in immunology2021
Type 2 Diabetes Mellitus and Latent Tuberculosis Infection Moderately Influence Innate Lymphoid Cell Immune Responses in Uganda.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Immune dysregulation in tuberculosis-diabetes comorbidity: mechanistic and translational insights.Frontiers in immunology · 2026Pooled it
- A quadral biosignature of IFN-γ, IL-2, IL-12 and IP-10 increases the diagnostic potential for latent tuberculosis among diabetic patients in Uganda.BMC immunology · 2025Article
- Metabolic dysfunction impairs Mycobacterium tuberculosis-specific cytokine and chemokine responses in latent tuberculosis and type 2 diabetes mellitus.Scientific reports · 2025Article
- Identification of circulating inflammation cytokines as a mediator of gut microbiota and type 2 diabetes mellitus: a Mendelian randomization study.Diabetology & metabolic syndrome · 2025Article
- Regulation of innate lymphoid cell by microbial metabolites.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Isoniazid preventive therapy modulates Mycobacterium tuberculosis-specific T-cell responses in individuals with latent tuberculosis and type 2 diabetes.Scientific reports · 2025Article
- Recent advances in biomarkers for diabetes mellitus and tuberculosis comorbidity: a comprehensive review.Frontiers in endocrinology · 2025Review
- Cost-effectiveness analysis of tuberculosis screening in diabetic patients in China: a decision-analytic Markov model.Frontiers in public health · 2025Article
- ImpairedFrontiers in immunology · 2024Article
- Gut microbiota composition can reflect immune responses of latent tuberculosis infection in patients with poorly controlled diabetes.Respiratory research · 2023Article
- Impact of diabetes mellitus on immunity to latent tuberculosis infection.Frontiers in clinical diabetes and healthcare · 2023Review
- The cause-effect relation of tuberculosis on incidence of diabetes mellitus.Frontiers in cellular and infection microbiology · 2023Review
- Immunologic, metabolic and genetic impact of diabetes on tuberculosis susceptibility.Frontiers in immunology · 2023Review
- ILC3: a case of conflicted identity.Frontiers in immunology · 2023Review
- Immunologic Role of Innate Lymphoid Cells againstBiomedicines · 2022Review
- Serial testing of latent tuberculosis infection in patients with diabetes mellitus using interferon-gamma release assay, tuberculin skin test, and creation tuberculin skin test.Frontiers in public health · 2022Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
Background: Type 2 diabetes mellitus (T2DM) is a major risk factor for the acquisition of latent tuberculosis (TB) infection (LTBI) and development of active tuberculosis (ATB), although the immunological basis for this susceptibility remains poorly characterised. Innate lymphoid cells (ILCs) immune responses to TB infection in T2DM comorbidity is anticipated to be reduced. We compared ILC responses (frequency and cytokine production) among adult patients with LTBI and T2DM to patients (13) with LTBI only (14), T2DM only (10) and healthy controls (11). Methods: Using flow cytometry, ILC phenotypes were categorised based on (Lin Results: Compared to healthy controls, patients with LTBI and T2DM had reduced frequencies of ILC2 and ILC3 respectively (median (IQR): 0.01 (0.005-0.04) and 0.002 (IQR; 0.002-0.007) and not ILC1 (0.04 (0.02-0.09) as expected. They also had increased production of IFN-γ [median (IQR): 17.1 (5.6-24.9)], but decreased production of IL-13 [19.6 (12.3-35.1)]. We however found that patients with T2DM had lower ILC cytokine responses in general but more marked for IL-22 production (median (IQR): IFN-γ 9.3 (4.8-22.6); IL-13 22.2 (14.7-39.7); IL-22 0.7 (IQR; 0.1-2.1) p-value 0.02), which highlights the immune suppression status of T2DM. We also found that poor glycaemic control altered ILC immune responses. Conclusion: This study demonstrates that LTBI and T2DM, and T2DM were associated with slight alterations of ILC immune responses. Poor T2DM control also slightly altered these ILC immune responses. Further studies are required to assess if these responses recover after treatment of either TB or T2DM.
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