Author
Listed:
- Cheryl L. Day
(Doris Duke Medical Research Institute, University of KwaZulu Natal
Massachusetts General Hospital and Division of AIDS, Harvard Medical School
The Peter Medawar Building for Pathogen Research, Oxford University)
- Daniel E. Kaufmann
(Massachusetts General Hospital and Division of AIDS, Harvard Medical School)
- Photini Kiepiela
(Doris Duke Medical Research Institute, University of KwaZulu Natal)
- Julia A. Brown
(Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School)
- Eshia S. Moodley
(Doris Duke Medical Research Institute, University of KwaZulu Natal)
- Sharon Reddy
(Doris Duke Medical Research Institute, University of KwaZulu Natal)
- Elizabeth W. Mackey
(Massachusetts General Hospital and Division of AIDS, Harvard Medical School)
- Joseph D. Miller
(Emory University School of Medicine
Immunology, Emory University School of Medicine)
- Alasdair J. Leslie
(The Peter Medawar Building for Pathogen Research, Oxford University)
- Chantal DePierres
(Doris Duke Medical Research Institute, University of KwaZulu Natal)
- Zenele Mncube
(Doris Duke Medical Research Institute, University of KwaZulu Natal)
- Jaikumar Duraiswamy
(Emory University School of Medicine
Immunology, Emory University School of Medicine)
- Baogong Zhu
(Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School)
- Quentin Eichbaum
(Massachusetts General Hospital and Division of AIDS, Harvard Medical School)
- Marcus Altfeld
(Massachusetts General Hospital and Division of AIDS, Harvard Medical School)
- E. John Wherry
(The Wistar Institute)
- Hoosen M. Coovadia
(Doris Duke Medical Research Institute, University of KwaZulu Natal)
- Philip J. R. Goulder
(Doris Duke Medical Research Institute, University of KwaZulu Natal
Massachusetts General Hospital and Division of AIDS, Harvard Medical School
The Peter Medawar Building for Pathogen Research, Oxford University)
- Paul Klenerman
(The Peter Medawar Building for Pathogen Research, Oxford University)
- Rafi Ahmed
(Emory University School of Medicine
Immunology, Emory University School of Medicine)
- Gordon J. Freeman
(Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School)
- Bruce D. Walker
(Doris Duke Medical Research Institute, University of KwaZulu Natal
Massachusetts General Hospital and Division of AIDS, Harvard Medical School
Howard Hughes Medical Institute)
Abstract
HIV and immunity Blocking a protein called PD-1 (programmed death 1) might provide a way to boost the immune function of T cells crippled by HIV infection. A study published earlier this year showed that blocking of PD-1 function in virally infected mice could restore the function of exhausted T cells and help fight infection. Now the phenomenon has been found to occur in humans. The T cells in HIV patients were found to have many more PD-1 receptors on their surface than is normal; the degree of PD-1 production correlates with markers of disease progression including the extent to which T cells are disabled and the levels of virus within the body. An antibody that blocks this receptor promotes the immune response to HIV in laboratory experiments, suggesting that a similar strategy might work to fight the disease in humans.
Suggested Citation
Cheryl L. Day & Daniel E. Kaufmann & Photini Kiepiela & Julia A. Brown & Eshia S. Moodley & Sharon Reddy & Elizabeth W. Mackey & Joseph D. Miller & Alasdair J. Leslie & Chantal DePierres & Zenele Mncu, 2006.
"PD-1 expression on HIV-specific T cells is associated with T-cell exhaustion and disease progression,"
Nature, Nature, vol. 443(7109), pages 350-354, September.
Handle:
RePEc:nat:nature:v:443:y:2006:i:7109:d:10.1038_nature05115
DOI: 10.1038/nature05115
Download full text from publisher
As the access to this document is restricted, you may want to search for a different version of it.
Citations
Citations are extracted by the
CitEc Project, subscribe to its
RSS feed for this item.
Cited by:
- Norma Rallón & Marcial García & Javier García-Samaniego & Alfonso Cabello & Beatriz Álvarez & Clara Restrepo & Sara Nistal & Miguel Górgolas & José M Benito, 2018.
"Expression of PD-1 and Tim-3 markers of T-cell exhaustion is associated with CD4 dynamics during the course of untreated and treated HIV infection,"
PLOS ONE, Public Library of Science, vol. 13(3), pages 1-14, March.
- Becca Asquith, 2008.
"The Evolutionary Selective Advantage of HIV-1 Escape Variants and the Contribution of Escape to the HLA-Associated Risk of AIDS Progression,"
PLOS ONE, Public Library of Science, vol. 3(10), pages 1-10, October.
Corrections
All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:nature:v:443:y:2006:i:7109:d:10.1038_nature05115. See general information about how to correct material in RePEc.
If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.
We have no bibliographic references for this item. You can help adding them by using this form .
If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.
For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .
Please note that corrections may take a couple of weeks to filter through
the various RePEc services.