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AIDS/HIV

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Transcutaneous immunization induces mucosal CTLs and protective immunity by migration of primed skin dendritic cells
Igor M. Belyakov, … , Gregory M. Glenn, Jay A. Berzofsky
Igor M. Belyakov, … , Gregory M. Glenn, Jay A. Berzofsky
Published April 1, 2004
Citation Information: J Clin Invest. 2004;113(7):998-1007. https://doi.org/10.1172/JCI20261.
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Transcutaneous immunization induces mucosal CTLs and protective immunity by migration of primed skin dendritic cells

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Abstract

Transcutaneous immunization (TCI), the application of vaccines on the skin, induces robust systemic and mucosal antibodies in animal models and in humans. The means by which mucosal immune responses to vaccine antigens are elicited by TCI has not been well characterized. We examined the effect of TCI with an HIV peptide vaccine on the induction of mucosal and systemic CTL responses and protective immunity against mucosal challenge with live virus in mice. Robust HIV-specific CTL responses in the spleen and in the gut mucosa were detected after TCI. The responses were dependent upon the addition of an adjuvant and resulted in protection against mucosal challenge with recombinant vaccinia virus encoding HIV gp160. Although it is clear that adjuvant-activated DCs migrated mainly to draining lymph nodes, coculture with specific T cells and flow cytometry studies with DCs isolated from Peyer’s patches after TCI suggested that activated DCs carrying skin-derived antigen also migrated from the skin to immune-inductive sites in gut mucosa and presented antigen directly to resident lymphocytes. These results and previous clinical trial results support the observation that TCI is a safe and effective strategy for inducing strong mucosal antibody and CTL responses.

Authors

Igor M. Belyakov, Scott A. Hammond, Jeffrey D. Ahlers, Gregory M. Glenn, Jay A. Berzofsky

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Blockade of T cell costimulation reveals interrelated actions of CD4+ and CD8+ T cells in control of SIV replication
David A. Garber, … , Silvija I. Staprans, Mark B. Feinberg
David A. Garber, … , Silvija I. Staprans, Mark B. Feinberg
Published March 15, 2004
Citation Information: J Clin Invest. 2004;113(6):836-845. https://doi.org/10.1172/JCI19442.
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Blockade of T cell costimulation reveals interrelated actions of CD4+ and CD8+ T cells in control of SIV replication

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Abstract

In vivo blockade of CD28 and CD40 T cell costimulation pathways during acute simian immunodeficiency virus (SIV) infection of rhesus macaques was performed to assess the relative contributions of CD4+ T cells, CD8+ T cells, and Ab responses in modulating SIV replication and disease progression. Transient administration of CTLA4-Ig and anti–CD40L mAb to SIV-infected rhesus macaques resulted in dramatic inhibition of the generation of both SIV-specific cellular and humoral immune responses. Acute levels of proliferating CD8+ T cells were associated with early control of SIV viremia but did not predict ensuing set point viremia or survival. The level of in vivo CD4+ T cell proliferation during acute SIV infection correlated with concomitant peak levels of SIV plasma viremia, whereas measures of in vivo CD4+ T cell proliferation that extended into chronic infection correlated with lower SIV viral load and increased survival. These results suggest that proliferating CD4+ T cells function both as sources of virus production and as antiviral effectors and that increased levels of CD4+ T cell proliferation during SIV infections reflect antigen-driven antiviral responses rather than a compensatory homeostatic response. These results highlight the interrelated actions of CD4+ and CD8+ T cell responses in vivo that modulate SIV replication and pathogenesis.

Authors

David A. Garber, Guido Silvestri, Ashley P. Barry, Andrew Fedanov, Natalia Kozyr, Harold McClure, David C. Montefiori, Christian P. Larsen, John D. Altman, Silvija I. Staprans, Mark B. Feinberg

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HIV protease inhibitors promote atherosclerotic lesion formation independent of dyslipidemia by increasing CD36-dependent cholesteryl ester accumulation in macrophages
James Dressman, … , Melinda E. Wilson, Eric J. Smart
James Dressman, … , Melinda E. Wilson, Eric J. Smart
Published February 1, 2003
Citation Information: J Clin Invest. 2003;111(3):389-397. https://doi.org/10.1172/JCI16261.
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HIV protease inhibitors promote atherosclerotic lesion formation independent of dyslipidemia by increasing CD36-dependent cholesteryl ester accumulation in macrophages

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Abstract

Protease inhibitors decrease the viral load in HIV patients, however the patients develop hypertriglyceridemia, hypercholesterolemia, and atherosclerosis. It has been assumed that protease inhibitor–dependent increases in atherosclerosis are secondary to the dyslipidemia. Incubation of THP-1 cells or human PBMCs with protease inhibitors caused upregulation of CD36 and the accumulation of cholesteryl esters. The use of CD36-blocking antibodies, a CD36 morpholino, and monocytes isolated from CD36 null mice demonstrated that protease inhibitor–induced increases in cholesteryl esters were dependent on CD36 upregulation. These data led to the hypothesis that protease inhibitors induce foam cell formation and consequently atherosclerosis by upregulating CD36 and cholesteryl ester accumulation independent of dyslipidemia. Studies with LDL receptor null mice demonstrated that low doses of protease inhibitors induce an increase in the level of CD36 and cholesteryl ester in peritoneal macrophages and the development of atherosclerosis without altering plasma lipids. Furthermore, the lack of CD36 protected the animals from protease inhibitor–induced atherosclerosis. Finally, ritonavir increased PPAR-γ and CD36 mRNA levels in a PKC- and PPAR-γ–dependent manner. We conclude that protease inhibitors contribute to the formation of atherosclerosis by promoting the upregulation of CD36 and the subsequent accumulation of sterol in macrophages.

Authors

James Dressman, Jeanie Kincer, Sergey V. Matveev, Ling Guo, Richard N. Greenberg, Theresa Guerin, David Meade, Xiang-An Li, Weifei Zhu, Annette Uittenbogaard, Melinda E. Wilson, Eric J. Smart

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Collagen deposition in HIV-1 infected lymphatic tissues and T cell homeostasis
Timothy W. Schacker, … , Cavan Reilly, Ashley T. Haase
Timothy W. Schacker, … , Cavan Reilly, Ashley T. Haase
Published October 15, 2002
Citation Information: J Clin Invest. 2002;110(8):1133-1139. https://doi.org/10.1172/JCI16413.
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Collagen deposition in HIV-1 infected lymphatic tissues and T cell homeostasis

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Abstract

Research Article

Authors

Timothy W. Schacker, Phuong L. Nguyen, Gregory J. Beilman, Steven Wolinsky, Matthew Larson, Cavan Reilly, Ashley T. Haase

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Insight into CD8+ T cell expansion during HIV-1 infection
Souheil-Antoine Younes and colleagues provide evidence that IL-15 is involved in the expansion of CD8+ T cells in chronic HIV infection...
Published June 20, 2016
Scientific Show StopperAIDS/HIV

Designer proteins to hunt and kill latent HIV-1
Julia Sung, Joy Pickeral, Liquin Liu and colleagues developed designer proteins that detect and destroy rare populations of HIV-infected cells…
Published September 28, 2015
Scientific Show StopperAIDS/HIV
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