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Your search keyword '"Kjær, Kathrine"' showing total 8 results
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8 results on '"Kjær, Kathrine"'

3. TLR9 agonist MGN1703 enhances B cell differentiation and function in lymph nodes

Author

Schleimann, Mariane H., primary, Kobberø, Maria-Louise, additional, Vibholm, Line K., additional, Kjær, Kathrine, additional, Giron, Leila B., additional, Busman-Sahay, Kathleen, additional, Chan, Chi Ngai, additional, Nekorchuk, Michael, additional, Schmidt, Manuel, additional, Wittig, Burghardt, additional, Damsgaard, Tine E., additional, Ahlburg, Peter, additional, Hellfritzsch, Michel B., additional, Zuwala, Kaja, additional, Rothemejer, Frederik H., additional, Olesen, Rikke, additional, Schommers, Phillipp, additional, Klein, Florian, additional, Dweep, Harsh, additional, Kossenkov, Andrew, additional, Nyengaard, Jens R., additional, Estes, Jacob D., additional, Abdel-Mohsen, Mohamed, additional, Østergaard, Lars, additional, Tolstrup, Martin, additional, Søgaard, Ole S., additional, and Denton, Paul W., additional

Published
2019
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6. Histone Deacetylase Inhibitor Romidepsin Inhibits De Novo HIV-1 Infections

Author

Jønsson, Kasper L., primary, Tolstrup, Martin, additional, Vad-Nielsen, Johan, additional, Kjær, Kathrine, additional, Laustsen, Anders, additional, Andersen, Morten N., additional, Rasmussen, Thomas A., additional, Søgaard, Ole S., additional, Østergaard, Lars, additional, Denton, Paul W., additional, and Jakobsen, Martin R., additional

Published
2015
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7. Histone Deacetylase Inhibitor Romidepsin Inhibits De NovoHIV-1 Infections

Author

Jønsson, Kasper L., Tolstrup, Martin, Vad-Nielsen, Johan, Kjær, Kathrine, Laustsen, Anders, Andersen, Morten N., Rasmussen, Thomas A., Søgaard, Ole S., Østergaard, Lars, Denton, Paul W., and Jakobsen, Martin R.

Abstract

ABSTRACTAdjunct therapy with the histone deacetylase inhibitor (HDACi) romidepsin increases plasma viremia in HIV patients on combination antiretroviral therapy (cART). However, a potential concern is that reversing HIV latency with an HDACi may reactivate the virus in anatomical compartments with suboptimal cART concentrations, leading to de novoinfection of susceptible cells in these sites. We tested physiologically relevant romidepsin concentrations known to reactivate latent HIV in order to definitively address this concern. We found that romidepsin significantly inhibited HIV infection in peripheral blood mononuclear cells and CD4+T cells but not in monocyte-derived macrophages. In addition, romidepsin impaired HIV spreading in CD4+T cell cultures. When we evaluated the impact of romidepsin on quantitative viral outgrowth assays with primary resting CD4+T cells, we found that resting CD4+T cells exposed to romidepsin exhibited reduced proliferation and viability. This significantly lowered assay sensitivity when measuring the efficacy of romidepsin as an HIV latency reversal agent. Altogether, our data indicate that romidepsin-based HIV eradication strategies are unlikely to reseed a latent T cell reservoir, even under suboptimal cART conditions, because romidepsin profoundly restricts de novoHIV infections.

Published
2015
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8. Multiple Homozygous Variants in the STING-Encoding TMEM173 Gene in HIV Long-Term Nonprogressors.

Author

Tolstrup, Martin, Nissen, Sara K., Kjær, Kathrine, Mogensen, Trine H., Pedersen, Jesper G., Thavachelvam, Karthiga, Jakobsen, Martin R., Obel, Niels, and Helleberg, Marie

Subjects
*HIV-positive persons, *HIV infection genetics, *SINGLE nucleotide polymorphisms, *PROGRESSION-free survival, *VIRAL load, *IMMUNE response
Abstract

Among HIV-infected individuals, long-term nonprogressor (LTNP) patients experience slow CD4 T cell decline and almost undetectable viral load for several years after primary acquisition of HIV. Type I IFN has been suggested to play a pathogenic role in HIV pathogenesis, and therefore diminished IFN responses may underlie the LTNP phenotype. In this study, we examined the presence and possible immunological role of multiple homozygous single-nucleotide polymorphisms in the stimulator of IFN genes (STING) encoding gene TMEM173 involved in IFN induction and T cell proliferation in HIV LTNP patients. We identified LTNPs through the Danish HIV Cohort and performed genetic analysis by Sanger sequencing, covering the R71H-G230A-R293Q (HAQ) single-nucleotide polymorphisms in TMEM173. This was followed by investigation of STING mRNA and protein accumulation as well as innate immune responses and proliferation following STING stimulation and infection with replication-competent HIV in human blood-derived cells. We identified G230A-R293Q/G230A-R293Q and HAQ/HAQ homozygous TMEM173 variants in 2 out of 11 LTNP patients. None of the 11 noncontrollers on antiretroviral treatment were homozygous for these variants. We found decreased innate immune responses to DNA and HIV as well as reduced STING-dependent inhibition of CD4 T cell proliferation, particularly in the HAQ/HAQ HIV LTNP patients, compared with the age- and gender-matched noncontrollers on antiretroviral treatment. These findings suggest that homozygous HAQ STING variants contribute to reduced inhibition of CD4 T cell proliferation and a reduced immune response toward DNA and HIV, which might result in reduced levels of constitutive IFN production. Consequently, the HAQ/HAQ TMEM173 genotype may contribute to the slower disease progression characteristic of LTNPs. [ABSTRACT FROM AUTHOR]

Published
2018
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