ArticleJournal of clinical immunology2005
Mechanisms of apoptosis of T-cells in human tuberculosis.
Article in Journal of clinical immunology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed, 36 citations in OpenAlex.
- CD4 lymphocyte dynamics in Tanzanian pulmonary tuberculosis patients with and without HIV co-infection.BMC infectious diseases · 2012Trial
- CDK1‑induced regulation of p53 phosphorylation at Ser315 mediates cell cycle arrest and apoptosis of macrophages infected with clinical isolates ofMolecular medicine reports · 2026Article
- Host Cell Death and Modulation of Immune Response againstInternational journal of molecular sciences · 2024Review
- Possible Mechanisms of Lymphopenia in Severe Tuberculosis.Microorganisms · 2023Review
- Single-cell profiling reveals distinct immune response landscapes in tuberculous pleural effusion and non-TPE.Frontiers in immunology · 2023Article
- Downmodulation of Regulatory T Cells Producing TGF-β Participates in Pathogenesis of Leprosy Reactions.Frontiers in medicine · 2022Article
- A Sex-Stratified Genome-Wide Association Study of Tuberculosis Using a Multi-Ethnic Genotyping Array.Frontiers in genetics · 2018Article
- HIV-1 Infection Is Associated with Depletion and Functional Impairment ofJournal of immunology (Baltimore, Md. : 1950) · 2017Article
- Bacterial subversion of cAMP signalling inhibits cathelicidin expression, which is required for innate resistance to Mycobacterium tuberculosis.The Journal of pathology · 2017Article
- Article
- The within host dynamics of Mycobacterium avium ssp. paratuberculosis infection in cattle: where time and place matter.Veterinary research · 2015Review
- Adequate Th2-type response associates with restricted bacterial growth in latent mycobacterial infection of zebrafish.PLoS pathogens · 2014Article
- Article
- Expression of TNF-alpha-dependent apoptosis-related genes in the peripheral blood of Malagasy subjects with tuberculosis.PloS one · 2013Article
- Cytotoxic activity of dendritic cells as a possible mechanism of negative regulation of T lymphocytes in pulmonary tuberculosis.Clinical & developmental immunology · 2012Article
- Article
- Immunoregulation in TB: observations and implications.Clinical and translational science · 2010Review
- Differences in virulence and immune response induced in a murine model by isolates of Mycobacterium ulcerans from different geographic areas.Clinical and experimental immunology · 2009Article
- Comparative evaluation of cytokines, T-cell apoptosis, and costimulatory molecule expression in tuberculous and nontuberculous pleurisy.Clinical and translational science · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 7 institutions in 2 countries.
Funding
Abstract
The role of TGF-beta TNF-alpha FasL and Bcl-2 in apoptosis of CD4 T-cells during active TB was studied. Coculture of PBMC from TB patients with neutralizing antibodies to TGF-beta or TNF-alpha decreased spontaneous (P < or = 0.05) and MTB-induced (P < or = 0.02) T-cell apoptosis by 50-90%, but effects were not additive. Interestingly, only levels of TGF-beta in supernatants correlated with rates of spontaneous and MTB-induced apoptosis. FasL surface and mRNA expression were higher in unstimulated and MTB-stimulated PBMC from patients than controls, and neutralization of FasL abrogated apoptosis of T-cells from patients only. Intracellular Bcl-2 protein was lower among unstimulated CD4 T-cells from patients than those from controls (P < or = 0.02), and MTB stimulation reduced intracellular Bcl-2 content in CD4 T-cells from patients only (P < or = 0.001). These findings may indicate that, during TB, predisposition of CD4 T-cells to apoptosis may involve both low expression of Bcl-2, and excessive expression of TGF-beta TNF-alpha and FasL.
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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.