Transcriptional Profiling of Dysregulated lncRNAs in B cells Response to Active Tuberculosis
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE89552 | GEO | 2017/01/30
SECONDARY ACCESSION(S): PRJNA352530
REPOSITORIES: GEO
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Project description:Individuals exposed to Mycobacterium tuberculosis (Mtb) may become infected and are classified as with latent tuberculosis infection (LTBI) and remain whole time life in this condition or develop active tuberculosis (TB). Among the multiple factors governing the outcome of the infection, dendritic cells (DC) play a major role in dictating protective immunity. However, current knowledge on the role of the diverse components of human DC in shaping specific T cell response during Mtb infection is limited. In this study, we performed a comparative evaluation of peripheral blood circulating DC subsets along with the functional capability of monocyte-derived IFN-α DC to induce Mtb antigen-specific T cell response in patients with active TB, subjects with LTBI and healthy donors (HD). The percentage of BDCA3+ mDC2 and CD123+ pDC declined significantly in active TB patients with respect HD whereas the same subsets displayed a remarkable activation in LTBI. Simultaneously, IFN-α-driven differentiation of DC resulted profoundly impaired from monocytes of active TB patients as compared to LTBI and HD individuals. Importantly, the specific altered developmental trait of IFN-α DC from active TB patients was associated with a marked change of molecular signalings conveying antigen presentation as well as full inability to induce antigen-specific T cell response. Thus, these data unravel an unavoidable role of IFN-α in determining the induction of Mtb-specific protective immunity which is essential to control Mtb infection.
2017-12-18 | GSE84344 | GEO
Project description:Tuberculosis (TB), caused by infection with Mycobacterium tuberculosis (M. tuberculosis), is a major cause of morbidity and mortality worldwide and efforts to control TB are hampered by difficulties with diagnosis, prevention and treatment. Most people infected with M. tuberculosis remain asymptomatic, termed latent TB, with a 10% lifetime risk of developing active TB disease, but current tests cannot identify which individuals will develop disease. The immune response to M. tuberculosis is complex and incompletely characterized, hindering development of new diagnostics, therapies and vaccines. The goals of this study include: 1. Identify a transcript signature for active TB in intermediate and high burden settings, correlating with radiological extent of disease and reverting to that of healthy controls following treatment; 2. Identify a specific transcript signature that discriminated active TB from other inflammatory and infectious diseases; 3. Classify TB signature using modular and pathway analysis tools.
2010-08-11 | GSE22098 | GEO
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2014-10-21 | E-GEOD-62525 | biostudies-arrayexpress
Project description:Tuberculosis (TB) is a serious infectious disease, but current methods of detection require improvement in sensitivity, efficiency or specificity. We conducted a microarray experiment, comparing the gene expression profiles in peripheral blood mononuclear cells among individuals with active TB, latent infection, and healthy conditions in a Taiwanese population. These differentially expressed genes may be potential biomarkers that can differentiate between active TB and latent infection.
2014-10-21 | GSE62525 | GEO
Project description:Tuberculosis (TB), caused by infection with Mycobacterium tuberculosis (M. tuberculosis), is a major cause of morbidity and mortality worldwide and efforts to control TB are hampered by difficulties with diagnosis, prevention and treatment. Most people infected with M. tuberculosis remain asymptomatic, termed latent TB, with a 10% lifetime risk of developing active TB disease, but current tests cannot identify which individuals will develop disease. The immune response to M. tuberculosis is complex and incompletely characterized, hindering development of new diagnostics, therapies and vaccines. The goals of this study include: 1. Identify a transcript signature for active TB in intermediate and high burden settings, correlating with radiological extent of disease and reverting to that of healthy controls following treatment; 2. Identify a specific transcript signature that discriminated active TB from other inflammatory and infectious diseases; 3. Classify TB signature using modular and pathway analysis tools. Three milliliters of whole blood was collected in Tempus tubes from 12 pediatric streptococcus, 40 pediatric staphylococcus, 31 still’s disease, 82 pediatric systemic lupus erythematosus (SLE) and 28 adult SLE patients. RNA was extracted and globin reduced. Labeled cRNA was hybridized to Illumina Human HT-12 Beadchips. Healthy controls were included to match patients’ demographic data. Genespring software was used to analyze active TB transcript signatures, comparing with healthy controls and other inflammatory and infectious diseases.
2010-08-11 | E-GEOD-22098 | biostudies-arrayexpress
Project description:Background: Mycobacterium tuberculosis infection is a leading cause of infectious death worldwide. Gene-expression microarray studies profiling the blood transcriptional response of tuberculosis (TB) patients have been undertaken in order to better understand the host immune response as well as to identify potential biomarkers of disease. To date most of these studies have focused on pulmonary TB patients with gene-expression profiles of extra-pulmonary TB patients yet to be compared to those of patients with pulmonary TB or sarcoidosis. Methods A novel cohort of patients with extra-pulmonary TB and sarcoidosis was recruited and the transcriptional response of these patients compared to those with pulmonary TB using a variety of transcriptomic approaches including testing a previously defined 380 gene meta-signature of active TB. Results The 380 meta-signature broadly differentiated active TB from healthy controls in this new dataset consisting of pulmonary and extra-pulmonary TB. The top 15 genes from this meta-signature had a lower sensitivity for differentiating extra-pulmonary TB from healthy controls as compared to pulmonary TB. We found the blood transcriptional responses in pulmonary and extra-pulmonary TB to be heterogeneous and to reflect the extent of symptoms of disease. Conclusions The transcriptional signature in extra-pulmonary TB demonstrated heterogeneity of gene expression reflective of symptom status, while the signature of pulmonary TB was distinct, based on a higher proportion of symptomatic individuals. These findings are of importance for the rational design and implementation of mRNA based TB diagnostics.
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Project description:Treatment of chronic inflammatory diseases with tumor necrosis factor alpha antagonists has been associated with increased risk of tuberculosis (TB). We examined the usefulness of the rabbit model of active pulmonary TB for studying the impact of the human immune modulatory reagent etanercept on the host immune response. Control of Mycobacterium tuberculosis (Mtb) infection, disease pathology and the global transcriptional response in Mtb-infected lungs of rabbits were studied. Etanercept treatment exacerbated disease pathology and reduced bacillary control in the lungs, compared to infected untreated animals. The microarray experiments involves comparison of changes in gene expression between Mtb-HN878 infected and Etanercept treated and untreated rabbit lungs at 4 and 8 weeks post-treatment, starting at 4 weeks post-infection.
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