GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    Monitoring clinical trials of therapeutic vaccines in HIV infection: role of treatment interruption
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Current Opinion in HIV and AIDS Vol. 2, No. 1 ( 2007-01), p. 56-61
    Details
    In: Current Opinion in HIV and AIDS, Ovid Technologies (Wolters Kluwer Health), Vol. 2, No. 1 ( 2007-01), p. 56-61
    Type of Medium: Online Resource
    ISSN: 1746-630X
    URL: Article
    DOI: 10.1097/COH.0b013e3280119264
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Activation of human immune cells with cowpea mosaic virus
    The American Association of Immunologists ; 2019
    In:  The Journal of Immunology Vol. 202, No. 1_Supplement ( 2019-05-01), p. 136.7-136.7
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 202, No. 1_Supplement ( 2019-05-01), p. 136.7-136.7
    Abstract: Novel approaches to retrieve and enhance immunity against cancer antigens have been established. One promising approach involves the use of virus particles derived from the plant virus, Cowpea Mosaic Virus (CPMV). Injection of CPMV into tumor stimulates systemic antitumor immunity in tumor mouse models and canine patients with tumors. The molecular pathways that account for these effects are not well defined. In these studies, we examine the capacity of CPMV to activate human monocytes. Peripheral blood mononuclear cells were incubated overnight with CPMV and CD14+ monocytes were examined by flow cytometry for expression of various markers. Cells were also incubated with “empty” (RNA-free) CPMV (eCPMV) for comparison. Responses to CPMV were also tested with THP-1 dual reporter cells, which are activated by various surface and cytoplasm pattern recognition receptors ligands except for TLR7. CPMV, but not eCPMV, mediated activation of human monocytes as indicated by induced expression of CD86, PDL-1, HLA-DR, IL-15R, and IP-10. In contrast to positive controls, PAM3CSK4 (TLR1/2 agonist) and LPS (TLR4 agonist), neither CPMV nor eCPMV induced activation of THP-1 cells. Activation of monocytes by CPMV was markedly inhibited by a chemical inhibitor of spleen tyrosine kinase (SYK), a key signaling component of TLR activation pathways. Effects of SYK inhibition were also observed in cells stimulated by a TLR7 agonist, imiquimod, but with different outcomes than CPMV stimulation, depending on the activation index that was assessed. These data demonstrate that CPMV activates monocytes in a manner that is highly dependent on RNA and SYK signaling. Overall, these data raise the possibility that TLR7 may play a role in CPMV adjuvant-like activity.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.202.Supp.136.7
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2019
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Predictors of SARS-CoV-2 RNA From Nasopharyngeal Swabs and Concordance With Other Compartments in Nonhospitalized Adults With Mild to Moderate COVID-19
    Oxford University Press (OUP) ; 2022
    In:  Open Forum Infectious Diseases Vol. 9, No. 11 ( 2022-11-02)
    Details
    In: Open Forum Infectious Diseases, Oxford University Press (OUP), Vol. 9, No. 11 ( 2022-11-02)
    Abstract: Identifying characteristics associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA shedding may be useful to understand viral compartmentalization, disease pathogenesis, and risks for viral transmission. Methods Participants were enrolled August 2020 to February 2021 in ACTIV-2/A5401, a placebo-controlled platform trial evaluating investigational therapies for mild-to-moderate coronavirus disease 2019 (COVID-19), and underwent quantitative SARS-CoV-2 RNA testing on nasopharyngeal and anterior nasal swabs, oral wash/saliva, and plasma at entry (day 0, pretreatment) and days 3, 7, 14, and 28. Concordance of RNA levels (copies/mL) across compartments and predictors of nasopharyngeal RNA levels were assessed at entry (n = 537). Predictors of changes over time were evaluated among placebo recipients (n = 265) with censored linear regression models. Results Nasopharyngeal and anterior nasal RNA levels at study entry were highly correlated (r = 0.84); higher levels of both were associated with greater detection of RNA in plasma and oral wash/saliva. Older age, White non-Hispanic race/ethnicity, lower body mass index (BMI), SARS-CoV-2 immunoglobulin G seronegativity, and shorter prior symptom duration were associated with higher nasopharyngeal RNA at entry. In adjusted models, body mass index and race/ethnicity associations were attenuated, but the association with age remained (for every 10 years older, mean nasopharyngeal RNA was 0.27 log10 copies/mL higher; P & lt; .001). Examining longitudinal viral RNA levels among placebo recipients, women had faster declines in nasopharyngeal RNA than men (mean change, −2.0 vs −1.3 log10 copies/mL, entry to day 3; P & lt; .001). Conclusions SARS-CoV-2 RNA shedding was concordant across compartments. Age was strongly associated with viral shedding, and men had slower viral clearance than women, which could explain sex differences in acute COVID-19 outcomes.
    Type of Medium: Online Resource
    ISSN: 2328-8957
    URL: Article
    DOI: 10.1093/ofid/ofac618
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2757767-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    Impact of Tamoxifen on Vorinostat-Induced Human Immunodeficiency Virus Expression in Women on Antiretroviral Therapy: AIDS Clinical Trials Group A5366, The MOXIE Trial
    Oxford University Press (OUP) ; 2022
    In:  Clinical Infectious Diseases Vol. 75, No. 8 ( 2022-10-12), p. 1389-1396
    Details
    In: Clinical Infectious Diseases, Oxford University Press (OUP), Vol. 75, No. 8 ( 2022-10-12), p. 1389-1396
    Abstract: Biological sex and the estrogen receptor alpha (ESR1) modulate human immunodeficiency virus (HIV) activity. Few women have enrolled in clinical trials of latency reversal agents (LRAs); their effectiveness in women is unknown. We hypothesized that ESR1 antagonism would augment induction of HIV expression by the LRA vorinostat. Methods AIDS Clinical Trials Group A5366 enrolled 31 virologically suppressed, postmenopausal women on antiretroviral therapy. Participants were randomized 2:1 to receive tamoxifen (arm A, TAMOX/VOR) or observation (arm B, VOR) for 5 weeks followed by 2 doses of vorinostat. Primary end points were safety and the difference between arms in HIV RNA induction after vorinostat. Secondary analyses included histone 4 acetylation, HIV DNA, and plasma viremia by single copy assay (SCA). Results No significant adverse events were attributed to study treatments. Tamoxifen did not enhance vorinostat-induced HIV transcription (between-arm ratio, 0.8; 95% confidence interval [CI], .2–2.4). Vorinostat-induced HIV transcription was higher in participants with increases in H4Ac (fold increase, 2.78; 95% CI, 1.34–5.79) vs those 9 who did n ot (fold increase, 1.04; 95% CI, .25–4.29). HIV DNA and SCA plasma viremia did not substantially change. Conclusions Tamoxifen did not augment vorinostat-induced HIV RNA expression in postmenopausal women. The modest latency reversal activity of vorinostat, postmenopausal status, and low level of HIV RNA expression near the limits of quantification limited assessment of the impact of tamoxifen. This study is the first HIV cure trial done exclusively in women and establishes both the feasibility and necessity of investigating novel HIV cure strategies in women living with HIV. Clinical Trials Registration NCT03382834.
    Type of Medium: Online Resource
    ISSN: 1058-4838 , 1537-6591
    URL: Article
    DOI: 10.1093/cid/ciac136
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2002229-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    Cytomegalovirus coinfection is associated with increased vascular-homing CD57+ CD4 T cells in HIV infection
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 225.38-225.38
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 225.38-225.38
    Abstract: Cytotoxic CD4 T cells are linked to cardiovascular morbidities and accumulate in both human immunodeficiency virus (HIV) and cytomegalovirus (CMV) infections, both of which are associated with increased risk of cardiovascular disease. Here we identify CMV coinfection as a major driver of the cytotoxic phenotype – characterized by elevated CD57 expression and reduced CD28 expression – in circulating CD4 T cells from people living with HIV infection (PLWH). We find that CD57+ CD4 T cells express high levels of the costimulatory receptor CD2 and that CD2/LFA-3 costimulation results in a more robust and polyfunctional effector response to T cell receptor (TCR) signals, compared to CD28-mediated costimulation. CD57+ CD4 T cells also express the vascular endothelium-homing receptor CX3CR1 and migrate toward CX3CL1-expressing endothelial cells in vitro. IL-15 promotes the cytotoxic phenotype, elevates CX3CR1 expression, and enhances the trafficking of CD57+ CD4 T cells, and may therefore be important in linking these cells to cardiovascular complications. Finally, we demonstrate the presence of CD57+ CD4 T cells and expression of IL-15, CX3CL1, and LFA-3 in atherosclerotic plaque tissues from HIV-uninfected donors. Our findings are consistent with a model in which cytotoxic CD4 T cells contribute to cardiovascular disease in HIV/CMV coinfection and in atherosclerosis via CX3CR1-mediated trafficking and CD2-mediated costimulation, and may help bridge the gap in understanding how CMV infection and immunity are linked to increased cardiovascular risk in PLWH.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.204.Supp.225.38
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 6
    Online Resource
    Online Resource
    Interferon-α differentially rescues CD4 and CD8 T cells from apoptosis in HIV infection
    Ovid Technologies (Wolters Kluwer Health) ; 2006
    In:  AIDS Vol. 20, No. 10 ( 2006-06-26), p. 1379-1389
    Details
    In: AIDS, Ovid Technologies (Wolters Kluwer Health), Vol. 20, No. 10 ( 2006-06-26), p. 1379-1389
    Type of Medium: Online Resource
    ISSN: 0269-9370
    URL: Article
    DOI: 10.1097/01.aids.0000233571.51899.ab
    RVK:
    XA 16838
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2006
    detail.hit.zdb_id: 2012212-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 7
    Online Resource
    Online Resource
    Diminished responsiveness to human β-defensin-3 and decreased TLR1 expression on monocytes and mDCs from HIV-1-infected patients
    Oxford University Press (OUP) ; 2012
    In:  Journal of Leukocyte Biology Vol. 92, No. 5 ( 2012-11-01), p. 1103-1109
    Details
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 92, No. 5 ( 2012-11-01), p. 1103-1109
    Abstract: Antigen-presenting cells from HIV-infected persons have impaired responses to hBD-3 stimulation, and reduced expression of TLR1, increasing susceptibility to mucosal infections. hBD-3 is an antimicrobial peptide that may contribute to adaptive immune responses by activating professional APCs via a TLR1/2-dependent mechanism. Patients with HIV disease experience increased susceptibility to mucosal infections, which may, in part, stem from diminished APC function. Our current studies demonstrate a reduced capacity of hBD-3 to induce the expression of a costimulatory molecule, CD80, on monocytes and mDCs from HIV-infected persons compared with cells from healthy controls. Although the expression of TLR1 and TLR2 on monocytes was not a strong predictor of hBD-3 responsiveness in bivariate analyses, monocytes and mDCs from HIV-infected persons expressed significantly lower levels of TLR1. Monocyte expression of the activation marker CD69, in cells from HIV-infected persons with therapeutically controlled viremia, was correlated directly with TLR2 and TLR4 expression but not with TLR1 expression. Overall, these studies suggest that immune activation may affect TLR2 and TLR4 expression but may not fully account for reduced TLR1 expression in monocytes from HIV-infected persons. Impairments in hBD-3 responsiveness and TLR1 expression are likely to contribute to increased risk of mucosal infection in HIV disease.
    Type of Medium: Online Resource
    ISSN: 1938-3673 , 0741-5400
    URL: Article
    DOI: 10.1189/jlb.1111555
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2012
    detail.hit.zdb_id: 2026833-6
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 8
    Online Resource
    Online Resource
    Membrane damage and repair in primary monocytes exposed to human β-defensin-3
    Oxford University Press (OUP) ; 2012
    In:  Journal of Leukocyte Biology Vol. 92, No. 5 ( 2012-11-01), p. 1083-1091
    Details
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 92, No. 5 ( 2012-11-01), p. 1083-1091
    Abstract: Human beta defensin-3 damages cell membranes of monocytes, potentially affecting these cellsˈ survival and activity at inflammation sites. Interactions of AMPs with plasma membranes of primary human immune cells are poorly characterized. Analysis of PI exclusion as a measure of membrane integrity indicated that hBD-3 caused membrane perturbations in monocytes but not T or B cells at concentrations typically used to kill bacteria or to induce activation of APCs. Bleb-like structures were observed in monocytes exposed to hBD-3. These cells also increased surface expression of LAMP1, a membrane repair marker after exposure to hBD-3. Furthermore, cell death was enhanced by adding an inhibitor of membrane repair. Removal of cholesterol from membranes resulted in greater susceptibility of cells to hBD-3, but cholesterol content was not different between the cell types, as assessed by filipin staining. Freshly isolated monocytes expressed higher levels of the negatively charged phospholipid, PS, on their outer leaflet compared with B or T cells. Preincubation of monocytes with molecules that bind PS protected these cells from hBD-3-induced membrane damage, suggesting that outer-membrane PS expression can at least partially explain monocyte susceptibility to hBD-3. The potential for membrane disruption caused by AMPs should be evaluated in various cell types when considering these molecules for therapeutic applications in humans.
    Type of Medium: Online Resource
    ISSN: 1938-3673 , 0741-5400
    URL: Article
    DOI: 10.1189/jlb.0112046
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2012
    detail.hit.zdb_id: 2026833-6
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 9
    Online Resource
    Online Resource
    Interferon- α inhibits CD4 T cell responses to interleukin-7 and interleukin-2 and selectively interferes with Akt signaling
    Oxford University Press (OUP) ; 2015
    In:  Journal of Leukocyte Biology Vol. 97, No. 6 ( 2015-06-01), p. 1139-1146
    Details
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 97, No. 6 ( 2015-06-01), p. 1139-1146
    Abstract: Persistent type I IFN production occurs during chronic viral infections, such as HIV disease. As type I IFNs have antiproliferative activity, it is possible that chronic exposure to these cytokines could adversely affect T cell homeostasis. We investigated the capacity of IFN-α to impair T cell proliferation induced by the homeostatic cytokine, IL-7, or another common γ-chain cytokine, IL-2, in cells from healthy human donors. We found that IL-7- or IL-2-induced proliferation of CD4+ T cells was partially inhibited in the presence of IFN-α. The CD4+ T cells that were exposed to IFN-α also displayed attenuated induction of IL-2 and CD40L following TCR stimulation. Analyses of signaling pathways indicated that IL-7 and IL-2 induced a delayed and sustained P-Akt signal that lasted for several days and was partially inhibited by IFN-α. In contrast, IL-7-induced P-STAT5 was not affected by IFN-α. Furthermore, IFN-α had no detectable effect on P-Akt that was induced by the chemokine SDF-1. Both inhibitors of P-Akt and P-STAT5 blocked IL-7-induced T cell proliferation, confirming that both signaling pathways are important for IL-7-induced T cell proliferation. These results demonstrate that IFN-α can selectively inhibit cytokine-induced P-Akt as a potential mechanism to disrupt homeostasis of T lymphocytes.
    Type of Medium: Online Resource
    ISSN: 0741-5400 , 1938-3673
    URL: Article
    DOI: 10.1189/jlb.4A0714-345RR
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2015
    detail.hit.zdb_id: 2026833-6
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 10
    Online Resource
    Online Resource
    CD56bright NK IL-7Rα expression negatively associates with HCV level, and IL-7-induced NK function is impaired during HCV and HIV infections
    Oxford University Press (OUP) ; 2017
    In:  Journal of Leukocyte Biology Vol. 102, No. 1 ( 2017-04-11), p. 171-184
    Details
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 102, No. 1 ( 2017-04-11), p. 171-184
    Abstract: Several lines of evidence support the concept that NK cells play an important role in control of hepatitis C virus (HCV) infection via cytokine secretion and cytotoxicity. IL-7 is a homeostatic cytokine with a role in T cell development, activation, proliferation, and cytokine secretion. The IL-7Rα chain [cluster of differentiation (CD)127] is expressed on NK cells, with greatest abundance on the CD56brightCD16dim/− (CD56bright) subset. Here, we measured CD127 expression on CD56bright, CD56dimCD16+ (CD56dim), or CD56negCD16+ (CD56neg) NK cell subsets of 25 uninfected donors (UD); 34 chronic HCV-infected, treatment-naiüve; 25 HIV-infected, virally suppressed on antiretroviral therapy (ART); and 42 HCV–HIV-coinfected subjects on ART. Interestingly, CD127 expression on CD56bright NK cells negatively correlated with HCV plasma levels in HCV monoinfection and HCV–HIV coinfection. IL-7 induced CD69 expression, as well as IFN-γ production, in CD56bright NK cells and also enhanced the IFN-α-induced CD69 expression on these cells. The latter was impaired in HIV infection. Furthermore, IL-7 induced B cell lymphoma 2 (BCL-2) expression and cell cycling of CD56bright NK cells, and this effect was impaired in HCV- and HIV-infected subjects. Whereas IL-7-stimulated CD56bright NK cell degranulation appeared intact in all cohorts, we observed impaired IL-7-activated NK cell cytolytic function in HCV- and HIV-infected subjects. Finally, IL-7-induced phosphorylation of STAT-5 (pSTAT-5) signa ling was impaired in NK cells of subjects with chronic viral infection, and this was reversible upon 6 mo of viral suppression with IFN-free HCV therapy. These results implicate that IL-7-dependent NK cell activation and effector function may be other host immune surveillance mechanisms that are impaired in viral infections.
    Type of Medium: Online Resource
    ISSN: 0741-5400 , 1938-3673
    URL: Article
    DOI: 10.1189/jlb.5A1116-456R
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2017
    detail.hit.zdb_id: 2026833-6
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...