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38 results on '"Ancuta, Petronela"'

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1. Altered memory CCR6 + Th17-polarised T-cell function and biology in people with HIV under successful antiretroviral therapy and HIV elite controllers.

3. Retinoic acid enhances HIV-1 reverse transcription and transcription in macrophages via mTOR-modulated mechanisms.

4. Genetic haute couture to block HIV-1 at front doors.

5. Alterations in Th17 Cells and Non-Classical Monocytes as a Signature of Subclinical Coronary Artery Atherosclerosis during ART-Treated HIV-1 Infection.

6. Identification of aryl hydrocarbon receptor as a barrier to HIV-1 infection and outgrowth in CD4 + T cells.

7. Targeting Th17 cells in HIV-1 remission/cure interventions.

8. Th17 cell master transcription factor RORC2 regulates HIV-1 gene expression and viral outgrowth.

9. Overt IL-32 isoform expression at intestinal level during HIV-1 infection is negatively regulated by IL-17A.

10. Antiretroviral Drug Transporters and Metabolic Enzymes in Circulating Monocytes and Monocyte-Derived Macrophages of ART-Treated People Living With HIV and HIV-Uninfected Individuals.

11. Peculiar Phenotypic and Cytotoxic Features of Pulmonary Mucosal CD8 T Cells in People Living with HIV Receiving Long-Term Antiretroviral Therapy.

12. Plasma Levels of C-Type Lectin REG3α and Gut Damage in People With Human Immunodeficiency Virus.

13. Upregulation of IL-32 Isoforms in Virologically Suppressed HIV-Infected Individuals: Potential Role in Persistent Inflammation and Transcription From Stable HIV-1 Reservoirs.

14. HIV-1 is rarely detected in blood and colon myeloid cells during viral-suppressive antiretroviral therapy.

15. The Biology of Monocytes and Dendritic Cells: Contribution to HIV Pathogenesis.

16. Host MicroRNAs-221 and -222 Inhibit HIV-1 Entry in Macrophages by Targeting the CD4 Viral Receptor.

17. Digoxin reveals a functional connection between HIV-1 integration preference and T-cell activation.

18. New insights into the heterogeneity of Th17 subsets contributing to HIV-1 persistence during antiretroviral therapy.

19. Identification of novel HIV-1 dependency factors in primary CCR4(+)CCR6(+)Th17 cells via a genome-wide transcriptional approach.

20. Nef promotes evasion of human immunodeficiency virus type 1-infected cells from the CTLA-4-mediated inhibition of T-cell activation.

21. Impaired Th17 polarization of phenotypically naive CD4(+) T-cells during chronic HIV-1 infection and potential restoration with early ART.

22. Transcriptional profiling reveals molecular signatures associated with HIV permissiveness in Th1Th17 cells and identifies peroxisome proliferator-activated receptor gamma as an intrinsic negative regulator of viral replication.

23. Down-regulation of CTLA-4 by HIV-1 Nef protein.

24. Memory CCR6+CD4+ T cells are preferential targets for productive HIV type 1 infection regardless of their expression of integrin β7.

25. Coreceptors and HIV-1 pathogenesis.

26. Th17 lineage commitment and HIV-1 pathogenesis.

27. Peripheral blood CCR4+CCR6+ and CXCR3+CCR6+CD4+ T cells are highly permissive to HIV-1 infection.

28. HIV reservoir size and persistence are driven by T cell survival and homeostatic proliferation.

29. Mechanisms of HIV-1 neurotropism.

30. CD16+ monocytes exposed to HIV promote highly efficient viral replication upon differentiation into macrophages and interaction with T cells.

31. HIV-1 is rarely detected in blood and colon myeloid cells during viral-suppressive antiretroviral therapy

33. Identification of aryl hydrocarbon receptor as a barrier to HIV-1 infection and outgrowth in CD4+ T cells.

34. The Th17 Lineage: From Barrier Surfaces Homeostasis to Autoimmunity, Cancer, and HIV-1 Pathogenesis.

35. Molecular characterization of Th17 lymphocytes and monocyte-derived dendritic cells in the context of HIV-1 infection

36. Rôle de l'autophagie dans la dissémination du VIH-1 par les cellules dendritiques dérivées des monocytes circulants

37. Étude du rôle de l'interleukine-32 dans l'infection à VIH-1

38. Mécanismes moléculaires de la réplication préférentielle du VIH-1 dans les cellules à polarisation Th1Th17 versus Th1 : rôle de PPARG dans la régulation négative de la réplication virale

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