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ACTG A5258 Clinical administration of chloroquine to HIV-infected patients receiving antiretroviral therapy to reduce immune activation

ABSTRACT: ACTG A5258, we asked whether chloroquine could reduce the immune activation in HIV infection posited to be driven by microbial TLR agonists, such as bacterial elements translocated from the gut and HIV-1 RNAs . We anticipate that blocking this activation pathway might interfere with events in pathogenesis leading to AIDS- and non-AIDS-related clinical manifestations of HIV disease.

ORGANISM(S): Homo sapiens

PROVIDER: GSE71064 | GEO | 2016/07/15

SECONDARY ACCESSION(S): PRJNA290207

REPOSITORIES: GEO

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ACTG A5258 Clinical administration of chloroquine to HIV-infected patients receiving antiretroviral therapy to reduce immune activation

Project description:ACTG A5258, we asked whether chloroquine could reduce the immune activation in HIV infection posited to be driven by microbial TLR agonists, such as bacterial elements translocated from the gut and HIV-1 RNAs . We anticipate that blocking this activation pathway might interfere with events in pathogenesis leading to AIDS- and non-AIDS-related clinical manifestations of HIV disease. Blood samples were taken from 20 individuals at week 0 (before treatement) and week 12. 10 individuals received chloroquine 250mg orally and 10 individuals received placebo.

2016-07-15 | E-GEOD-71064 | biostudies-arrayexpress

ACTG A5258 Clinical administration of chloroquine to patients with untreated chronic HIV infection to reduce immune activation

2016-07-15 | E-GEOD-71063 | biostudies-arrayexpress

ACTG A5258 Clinical administration of chloroquine to patients with untreated chronic HIV infection to reduce immune activation

2016-07-15 | GSE71063 | GEO

Potentiation of glucocorticoid signaling by chloroquine via inhibition of lysosomes

Project description:Anti-malaria drug chloroquine has been used as an anti-inflammatory agent for treating systemic lupus erythematosus and rheumatoid arthritis, without clear mechanism of action. Here we report that chloroquine potently inhibits the expression of proinflammatory cytokines through transrepression of glucocorticoid receptor (GR). Instead of direct binding to GR, chloroquine synergistically activates glucocorticoid signaling via inhibition of lysosomal functions. In mouse collagen induced arthritis model, chloroquine synergizes the therapeutic effects of glucocorticoid. Lysosomal inhibition by bafilomycin A1, an inhibitor of V-type ATPase, or by knockdown of transcription factor EB (TFEB), a master activator of lysosomal biogenesis, mimics the effects of chloroquine. These results reveal an unexpected regulation of glucocorticoid signaling by lysosomes and provide a mechanistic basis for treating inflammation and autoimmune diseases by combination of glucocorticoids and lysosomal inhibitors.

2012-01-18 | GSE24579 | GEO

Potentiation of glucocorticoid signaling by chloroquine via inhibition of lysosomes

2012-01-18 | E-GEOD-24579 | biostudies-arrayexpress

Clinical administration of chloroquine to HIV-infected patients that are untreated or receiving antiretroviral therapy

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

2016-07-15 | GSE71065 | GEO

Epigenetic Features of HIV-Induced T-Cell Exhaustion Persist Despite Early Antiretroviral Therapy

Project description:T cell dysfunction occurs early following HIV infection, impacting the emergence of non-AIDS morbidities and limiting curative efforts. ART initiated during primary HIV infection (PHI) can reverse this dysfunction, but the extent of recovery is unknown. We studied 66 HIV-infected individuals treated from early PHI with up to three years of ART. Compared with HIV-uninfected controls, CD4 and CD8 T cells from early HIV infection were characterised by T cell activation and increased expression of the immune checkpoint receptors (ICRs) PD1, Tim-3 and TIGIT. Three years of ART lead to partial – but not complete – normalisation of ICR expression, the dynamics of which varied for individual ICRs. For HIV-specific cells, epigenetic profiling of tetramer-sorted CD8 T cells revealed that epigenetic features of exhaustion typically seen in chronic HIV infection were already present early in PHI, and that ART initiation during PHI resulted in only a partial shift of the epigenome to one with more favourable memory characteristics. These findings suggest that although ART initiation during PHI results in significant immune reconstitution, there may be only partial resolution of HIV-related phenotypic and epigenetic changes.

2023-07-19 | GSE237729 | GEO

Chloroquine Target Identification with MS-CETSA

Project description:ITDR MS-CETSA was conducted on chloroquine-treated live parasites and lysate of P. falciparum trophozoites in order to identify potential drug protein targets.

2023-12-11 | PXD046662 | Pride

Clinical administration of chloroquine to HIV-infected patients that are untreated or receiving antiretroviral therapy

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-07-15 | E-GEOD-71065 | biostudies-arrayexpress

Transcriptomic analysis to identify genes associated with chloroquine-mediated radiosensitization of glioblastoma stem cells

Project description:Tumour suppressor p53 regulates hundreds of genes by either activating or repressing their transcription. p53-dependent transcription is activated by stress factors such as DNA damage, reactive oxygen species, hypoxia or oncogenic signaling. Lysosomotropic agent and DNA intercalating agent chloroquine has been implicated in sensitizing glioblastoma to radiation via p53 pathway. This study evaluates the effects of chloroquine in glioblastoma stem cells differing for the status of TP53 by using an integrated approach encompassing in vitro, in vivo and in silico methodologies to characterize the impacts of chloroquine on cell vitality, tumor-propagating capacity and gene expression. We used microarrays to identify the genes whose expression is influenced by DNA intercalator chloroquine (ClQ) in glioblastoma stem cells expressing wild type p53 (line #993), mutant p53 (line G112) or a p53 null line #1095. To compare chloroquine-associated transcriptomic changes with those induced by ionizing radiation (IR), samples of IR-treated line #993 ("#993_IR") were analyzed in parallel with ClQ-treated samples ("993_ClQ").

2023-08-04 | GSE225191 | GEO

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