Impaired cell surface expression of human CD1d by the formation of an HIV-1 Nef/CD1d complex
Virology, ISSN: 0042-6822, Vol: 337, Issue: 2, Page: 242-252
2005
- 80Citations
- 23Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations80
- Citation Indexes80
- 80
- CrossRef64
- Captures23
- Readers23
- 23
Article Description
The HIV-1 Nef protein causes a decrease in major histocompatibility complex (MHC) class I and CD4 molecule expression on the cell surface. To determine if Nef can affect components of the innate immune response, we assessed the ability of Nef to alter the cell surface expression of human CD1d. In cells co-expressing CD1d and Nef, a substantial reduction in the cell surface level of CD1d was observed, with a concomitant reduction in the activation of CD1d-restricted NKT cells. Nef had a minimal effect on the cell surface expression of a mutant CD1d molecule in which the last 6 or 10 amino acids of the cytoplasmic tail were deleted. Additionally, it was found that Nef physically interacted with wild-type (but not tail-deleted) CD1d. Therefore, one means by which HIV-1 may be able to establish a foothold in an infected individual is by directly interfering with the functional cell surface expression of CD1d.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0042682205002394; http://dx.doi.org/10.1016/j.virol.2005.04.020; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=20444366188&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/15916790; https://linkinghub.elsevier.com/retrieve/pii/S0042682205002394; https://dx.doi.org/10.1016/j.virol.2005.04.020
Elsevier BV
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