CXCR3 Expression Pattern on CD4+ T Cells and IP-10 Levels with Regard to the HIV-1 Reservoir in the Gut-Associated Lymphatic Tissue
暂无分享,去创建一个
D. Duffy | M. Müller-Trutwin | V. Bondet | C. Lehmann | M. Augustin | G. Fätkenheuer | S. Chon | F. Klein | M. Oette | I. Suárez | U. Sandaradura de Silva | E. Knops | E. Heger | C. Horn | D. Nierhoff | M. Ercanoglu | C. Vivaldi | H. Schäfer
[1] D. Duffy,et al. HIV DNA reservoir and elevated PD‐1 expression of CD4 T‐cell subsets particularly persist in the terminal ileum of HIV‐positive patients despite cART , 2021, HIV medicine.
[2] S. Kent,et al. CD73+ CD127high Long-Term Memory CD4 T Cells Are Highly Proliferative in Response to Recall Antigens and Are Early Targets in HIV-1 Infection , 2021, International journal of molecular sciences.
[3] B. Berkhout,et al. CD32+CD4+ T Cells Are Highly Enriched for HIV DNA and Can Support Transcriptional Latency , 2020, Cell reports.
[4] J. Izopet,et al. Increase of CXCR3+ T cells impairs Th17 cells recruitment in the small intestine mucosa through IFN-γ and IL-18 during treated HIV-1 infection. , 2019, The Journal of infectious diseases.
[5] M. Sitbon,et al. Cellular Metabolism Is a Major Determinant of HIV-1 Reservoir Seeding in CD4+ T Cells and Offers an Opportunity to Tackle Infection. , 2019, Cell metabolism.
[6] D. Hazuda,et al. PD-1 blockade potentiates HIV latency reversal ex vivo in CD4+ T cells from ART-suppressed individuals , 2019, Nature Communications.
[7] R. Apps,et al. Evidence that CD32a does not mark the HIV-1 latent reservoir , 2018, Nature.
[8] R. Siliciano,et al. The role of CD32 during HIV-1 infection , 2018, Nature.
[9] D. Hazuda,et al. CD32 is expressed on cells with transcriptionally active HIV but does not enrich for HIV DNA in resting T cells , 2018, Science Translational Medicine.
[10] W. Paxton,et al. Blood CXCR3+ CD4 T Cells Are Enriched in Inducible Replication Competent HIV in Aviremic Antiretroviral Therapy-Treated Individuals , 2018, Front. Immunol..
[11] C. Rouzioux,et al. Impact of early cART on HIV blood and semen compartments at the time of primary infection , 2017, PloS one.
[12] L. Hanna,et al. Pathophysiology of CD4+ T-Cell Depletion in HIV-1 and HIV-2 Infections , 2017, Front. Immunol..
[13] J. Martinez-Picado,et al. Sensitive quantification of the HIV-1 reservoir in gut-associated lymphoid tissue , 2017, PloS one.
[14] J. Mellors,et al. Levels of HIV-1 persistence on antiretroviral therapy are not associated with markers of inflammation or activation , 2017, PLoS pathogens.
[15] Y. Lévy,et al. CD32a is a marker of a CD4 T-cell HIV reservoir harbouring replication-competent proviruses , 2017, Nature.
[16] S. Lewin,et al. Human Immunodeficiency Virus Persistence and T-Cell Activation in Blood, Rectal, and Lymph Node Tissue in Human Immunodeficiency Virus–Infected Individuals Receiving Suppressive Antiretroviral Therapy , 2017, The Journal of infectious diseases.
[17] E. Bernasconi,et al. Impairment of CCR6+ and CXCR3+ Th Cell Migration in HIV-1 Infection Is Rescued by Modulating Actin Polymerization , 2017, The Journal of Immunology.
[18] J. Routy,et al. HIV persists in CCR6+CD4+ T cells from colon and blood during antiretroviral therapy , 2016, AIDS.
[19] J. Routy,et al. New insights into the heterogeneity of Th17 subsets contributing to HIV-1 persistence during antiretroviral therapy , 2016, Retrovirology.
[20] F. Barré-Sinoussi,et al. Elevated Basal Pre-infection CXCL10 in Plasma and in the Small Intestine after Infection Are Associated with More Rapid HIV/SIV Disease Onset , 2016, PLoS pathogens.
[21] S. Lewin,et al. Persistence of integrated HIV DNA in CXCR3 + CCR6 + memory CD4+ T cells in HIV-infected individuals on antiretroviral therapy , 2016, AIDS.
[22] A. Casrouge,et al. Inhibition of DPP4 activity in humans establishes its in vivo role in CXCL10 post‐translational modification: prospective placebo‐controlled clinical studies , 2016, EMBO molecular medicine.
[23] C. Tremblay,et al. Identification of novel HIV-1 dependency factors in primary CCR4+CCR6+Th17 cells via a genome-wide transcriptional approach , 2015, Retrovirology.
[24] William W. Agace,et al. Regional specialization within the intestinal immune system , 2014, Nature Reviews Immunology.
[25] F. Romerio,et al. Longitudinal analysis of distribution and function of plasmacytoid dendritic cells in peripheral blood and gut mucosa of HIV infected patients. , 2014, The Journal of infectious diseases.
[26] P. Lemey,et al. The HIV-1 reservoir in eight patients on long-term suppressive antiretroviral therapy is stable with few genetic changes over time , 2013, Proceedings of the National Academy of Sciences.
[27] D. Havlir,et al. The distribution of HIV DNA and RNA in cell subsets differs in gut and blood of HIV-positive patients on ART: implications for viral persistence. , 2013, The Journal of infectious diseases.
[28] Jeffrey N. Martin,et al. Comparison of HIV DNA and RNA in gut-associated lymphoid tissue of HIV-infected controllers and noncontrollers , 2013, AIDS.
[29] J. García,et al. Impact of highly active antiretroviral therapy initiation on CD4+ T-cell repopulation in duodenal and rectal mucosa , 2013, AIDS.
[30] D. Asmuth,et al. Gastrointestinal-associated lymphoid tissue immune reconstitution in a randomized clinical trial of raltegravir versus non-nucleoside reverse transcriptase inhibitor-based regimens , 2012, AIDS.
[31] C. Chougnet,et al. HIV-Induced T-Cell Activation/Exhaustion in Rectal Mucosa Is Controlled Only Partially by Antiretroviral Treatment , 2012, PloS one.
[32] C. B. Hare,et al. Differences in HIV burden and immune activation within the gut of HIV-positive patients receiving suppressive antiretroviral therapy. , 2010, The Journal of infectious diseases.
[33] G. Boucher,et al. Establishment of HIV-1 latency in resting CD4+ T cells depends on chemokine-induced changes in the actin cytoskeleton , 2010, Proceedings of the National Academy of Sciences.
[34] Geneviève Boucher,et al. HIV reservoir size and persistence are driven by T cell survival and homeostatic proliferation , 2009, Nature Medicine.
[35] Mario Roederer,et al. Emerging concepts in the immunopathogenesis of AIDS. , 2009, Annual review of medicine.
[36] Z. Sun,et al. The roles of CCR6 in migration of Th17 cells and regulation of effector T-cell balance in the gut , 2009, Mucosal Immunology.
[37] T. Chun,et al. Effective CD4+ T-cell restoration in gut-associated lymphoid tissue of HIV-infected patients is associated with enhanced Th17 cells and polyfunctional HIV-specific T-cell responses , 2008, Mucosal Immunology.
[38] D. Nickle,et al. Persistence of HIV in gut-associated lymphoid tissue despite long-term antiretroviral therapy. , 2008, The Journal of infectious diseases.
[39] S. Mehandru,et al. Role of the gastrointestinal tract in establishing infection in primates and humans , 2008, Current opinion in HIV and AIDS.
[40] M. Markowitz,et al. Lack of Mucosal Immune Reconstitution during Prolonged Treatment of Acute and Early HIV-1 Infection , 2006, PLoS medicine.
[41] D. Douek,et al. HIV disease: fallout from a mucosal catastrophe? , 2006, Nature Immunology.
[42] D. Price,et al. CD4+ T Cell Depletion during all Stages of HIV Disease Occurs Predominantly in the Gastrointestinal Tract , 2004, The Journal of experimental medicine.
[43] Christine Hogan,et al. Primary HIV-1 Infection Is Associated with Preferential Depletion of CD4+ T Lymphocytes from Effector Sites in the Gastrointestinal Tract , 2004, The Journal of experimental medicine.
[44] J. Flamm,et al. Severe CD4+ T-Cell Depletion in Gut Lymphoid Tissue during Primary Human Immunodeficiency Virus Type 1 Infection and Substantial Delay in Restoration following Highly Active Antiretroviral Therapy , 2003, Journal of Virology.
[45] D. Markovitz,et al. The C-X-C chemokine IP-10 stimulates HIV-1 replication. , 2003, Virology.
[46] J. Lisziewicz,et al. Latent infection of CD4+ T cells provides a mechanism for lifelong persistence of HIV-1, even in patients on effective combination therapy , 1999, Nature Medicine.
[47] J S Cornes,et al. Number, size, and distribution of Peyer's patches in the human small intestine , 1965, Gut.