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Mtb-induced BAL cell gene expression signature in LTBI [CD4 experiment]

ABSTRACT: Mtb-induced BAL cell gene expression signature in LTBI [CD4 experiment]

PROVIDER: PRJNA555590 | ENA |

REPOSITORIES: ENA

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Mtb-induced BAL cell gene expression signature in LTBI [CD4 experiment]

Project description:In this study, we evaluated global Mtb-induced gene expression in airway immune cells obtained by bronchoalveolar lavage of individuals with latent tuberculosis infection (LTBI) and in Mtb-naïve control subjects We used microarrays to detail the global programme of gene expression evaluating the impact of localized T cells subsets in the recall responses of individuals with LTBI

2019-08-09 | GSE134564 | GEO

Mtb-induced BAL cell gene expression signature in LTBI [CD8 experiment]

Project description:Mtb-induced BAL cell gene expression signature in LTBI [CD8 experiment]

| PRJNA555589 | ENA

Mtb-induced BAL cell gene expression signature in LTBI [naive experiment]

Project description:Mtb-induced BAL cell gene expression signature in LTBI [naive experiment]

| PRJNA555591 | ENA

Mtb-induced BAL cell gene expression signature in LTBI [naive experiment]

2019-08-09 | GSE134565 | GEO

Mtb-induced BAL cell gene expression signature in LTBI [CD8 experiment]

2019-08-09 | GSE134550 | GEO

Mtb-induced BAL cell gene expression signature in LTBI

Project description:Mtb-induced BAL cell gene expression signature in LTBI

| PRJNA555583 | ENA

Mtb-induced BAL cell gene expression signature in LTBI

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-08-09 | GSE134566 | GEO

Transcriptional signature of MAITs in LTBI

Project description:We applied a cell population transcriptomics strategy to sorted human memory CD8 T cells to define novel immune signatures of latent tuberculosis infection (LTBI) and understand the phenotype of tuberculosis (TB)-specific T cells. We found a 41-gene signature that could discriminate between memory CD8 T cells from healthy LTBI subjects and noninfected controls. The gene signature was dominated by genes known to be associated with mucosal associated invariant T cells (MAITs) and reflected the lower frequency of MAITs observed in individuals with LTBI. There was no evidence for a conventional CD8 T cell specific signature between the two cohorts. We therefore investigated the MAITs in more detail in these cohorts. Phenotyping based on Vα7.2 and CD161 expression and MR1 tetramers revealed 2 distinct populations of CD8+Vα7.2+CD161+ T cells: MR1 tetramer+ and MR1 tetramer−, both of which had a distinct gene expression profile compared to CD8 memory T cells. Transcriptomic analysis of LTBI vs. noninfected individuals did not reveal significant differences for MR1 tetramer+ cells. However, gene expression of MR1 tetramer− cells showed a very different profile with large inter-individual diversity and a TB-specific signature. This was further strengthened by a more diverse TCR-α and -β repertoire of MR1 tetramer− cells as compared to MR1 tetramer+. Thus, cell population transcriptomics revealed a dominant MAIT signature in CD8 memory T cells that upon detailed investigation provided novel insights into the phenotype of different MAIT populations implicated in tuberculosis.

2020-05-13 | GSE132790 | GEO

Transcriptional signature of MAITs in LTBI

Project description:Transcriptional signature of MAITs in LTBI

| PRJNA549010 | ENA

System-wide identification of myeloid markers of TB disease and HIV-induced reactivation in the macaque model of Mtb infection and Mtb/SIV co-infection

Project description:Mycobacterium tuberculosis (Mtb) has developed specialized mechanisms to parasitize its host cell, the macrophage. These mechanisms allow it to overcome killing by oxidative burst and persist in the wake of an inflammatory response. Mtb infection in the majority of those exposed is controlled in an asymptomatic form referred to as latent tuberculosis infection (LTBI). HIV is a well-known catalyst of reactivation of LTBI to active TB infection (ATB). Through the use of nonhuman primates (NHPs) co-infected with Mtb and Simian Immunodeficiency Virus (Mtb/SIV), we are able to simulate human progression of TB/AIDS comorbidity. The advantage of NHP models is that they recapitulate the breadth of human TB outcomes, including immune control of infection, and loss of this control due to SIV co-infection. Using macaques infected with Mtb or Mtb/SIV and with different clinical outcomes we attempted to identify signatures between those that progress to active infection after SIV challenge (reactivators) and those that control the infection (non-reactivators).

2022-09-23 | GSE213850 | GEO

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