Institution
Vaccine Research Center
About: Vaccine Research Center is a based out in . It is known for research contribution in the topics: Immune system & Antibody. The organization has 666 authors who have published 808 publications receiving 55230 citations. The organization is also known as: Dale and Betty Bumpers Vaccine Research Center & VRC.
Topics: Immune system, Antibody, T cell, Epitope, Vaccination
Papers published on a yearly basis
Papers
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TL;DR: There remains a need for improved adjuvants that enhance protective antibody responses, especially in populations that respond poorly to current vaccines, and the larger challenge is to develop vaccines that generate strong T cell immunity with purified or recombinant vaccine antigens.
1,556 citations
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TL;DR: The quality of a CD4+ T-cell cytokine response can be a crucial determinant in whether a vaccine is protective, and may provide a new and useful prospective immune correlate of protection for vaccines based on T-helper type 1 (TH1) cells.
Abstract: CD4+ T cells have a crucial role in mediating protection against a variety of pathogens through production of specific cytokines. However, substantial heterogeneity in CD4+ T-cell cytokine responses has limited the ability to define an immune correlate of protection after vaccination. Here, using multiparameter flow cytometry to assess the immune responses after immunization, we show that the degree of protection against Leishmania major infection in mice is predicted by the frequency of CD4+ T cells simultaneously producing interferon-gamma, interleukin-2 and tumor necrosis factor. Notably, multifunctional effector cells generated by all vaccines tested are unique in their capacity to produce high amounts of interferon-gamma. These data show that the quality of a CD4+ T-cell cytokine response can be a crucial determinant in whether a vaccine is protective, and may provide a new and useful prospective immune correlate of protection for vaccines based on T-helper type 1 (TH1) cells.
1,308 citations
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TL;DR: The findings show that HIV-specific CD4+ T cells are preferentially infected by HIV in vivo, which provides a potential mechanism to explain the loss of HIV- specific CD4- T-cell responses, and consequently theloss of immunological control of HIV replication.
Abstract: HIV infection is associated with the progressive loss of CD4(+) T cells through their destruction or decreased production. A central, yet unresolved issue of HIV disease is the mechanism for this loss, and in particular whether HIV-specific CD4(+) T cells are preferentially affected. Here we show that HIV-specific memory CD4(+) T cells in infected individuals contain more HIV viral DNA than other memory CD4(+) T cells, at all stages of HIV disease. Additionally, following viral rebound during interruption of antiretroviral therapy, the frequency of HIV viral DNA in the HIV-specific pool of memory CD4(+) T cells increases to a greater extent than in memory CD4(+) T cells of other specificities. These findings show that HIV-specific CD4(+) T cells are preferentially infected by HIV in vivo. This provides a potential mechanism to explain the loss of HIV-specific CD4(+) T-cell responses, and consequently the loss of immunological control of HIV replication. Furthermore, the phenomenon of HIV specifically infecting the very cells that respond to it adds a cautionary note to the practice of structured therapy interruption.
1,283 citations
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TL;DR: The data demonstrate that over one-half of all memory CD4+ T cells in SIV-infected macaques are destroyed directly by viral infection during the acute phase—an insult that certainly heralds subsequent immunodeficiency.
Abstract: It has recently been established that both acute human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) infections are accompanied by a dramatic and selective loss of memory CD4+ T cells predominantly from the mucosal surfaces. The mechanism underlying this depletion of memory CD4+ T cells (that is, T-helper cells specific to previously encountered pathogens) has not been defined. Using highly sensitive, quantitative polymerase chain reaction together with precise sorting of different subsets of CD4+ T cells in various tissues, we show that this loss is explained by a massive infection of memory CD4+ T cells by the virus. Specifically, 30-60% of CD4+ memory T cells throughout the body are infected by SIV at the peak of infection, and most of these infected cells disappear within four days. Furthermore, our data demonstrate that the depletion of memory CD4+ T cells occurs to a similar extent in all tissues. As a consequence, over one-half of all memory CD4+ T cells in SIV-infected macaques are destroyed directly by viral infection during the acute phase-an insult that certainly heralds subsequent immunodeficiency. Our findings point to the importance of reducing the cell-associated viral load during acute infection through therapeutic or vaccination strategies.
1,260 citations
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TL;DR: The phase 1, dose-escalation, open-label trial of a messenger RNA vaccine, mRNA-1273, which encodes the stabilized prefusion SARS-CoV-2 spike protein in healthy adults found it induced higher binding- and neutralizing-antibody titers than the 25-μg dose, which supports the use of the 100- μg dose in a phase 3 vaccine trial.
Abstract: Background Testing of vaccine candidates to prevent infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in an older population is important, since increased inciden...
1,136 citations
Authors
Showing all 666 results
Name | H-index | Papers | Citations |
---|---|---|---|
David Price | 138 | 1687 | 93535 |
Gary J. Nabel | 133 | 497 | 58611 |
John R. Mascola | 131 | 575 | 61581 |
Richard A. Koup | 122 | 401 | 61738 |
Mario Roederer | 117 | 406 | 50586 |
Daniel C. Douek | 113 | 376 | 44694 |
Barney S. Graham | 113 | 521 | 51124 |
Peter D. Kwong | 108 | 436 | 51150 |
Norman L. Letvin | 105 | 549 | 44245 |
James R. Johnson | 100 | 540 | 36994 |
Richard T. Wyatt | 84 | 190 | 33316 |
Lawrence Shapiro | 82 | 253 | 25142 |
Bali Pulendran | 81 | 218 | 33564 |
Robert A. Seder | 79 | 224 | 29442 |
Eric Hunter | 77 | 472 | 23653 |