CD26 up-regulates expression of CD86 on antigen-presenting cells by means of caveolin-1
Proceedings of the National Academy of Sciences of the United States of America, ISSN: 0027-8424, Vol: 101, Issue: 39, Page: 14186-14191
2004
- 109Citations
- 65Captures
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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.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations109
- Citation Indexes109
- 109
- CrossRef90
- Captures65
- Readers65
- 65
Article Description
CD26 is a T cell costimulatory molecule with dipeptidyl peptidase IV activity in its extracellular region. We previously reported that recombinant soluble CD26 enhanced T cell proliferation induced by the recall antigen tetanus toxoid (TT). However, the mechanism involved in this enhancement is not yet elucidated. We now demonstrate that CD26 binds Caveolin-1 on antigen-presenting cells, and that residues 201-211 of CD26 along with the serine catalytic site at residue 630 contribute to binding to caveolin-1 scaffolding domain. In addition, after CD26-caveolin-1 interaction on TT-loaded monocytes, caveolin-1 is phosphorylated, which links to activate NF-κB, followed by up-regulation of CD86. Finally, reduced caveolin-1 expression on monocytes inhibits CD26-mediated CD86 up-regulation and abrogates CD26 effect on TT-induced T cell proliferation. Taken together, these results strongly suggest that CD26-caveolin-1 interaction plays a role in the up-regulation of CD86 on TT-loaded monocytes and subsequent engagement with CD28 on T cells, leading to antigen-specific T cell activation.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=4644325083&origin=inward; http://dx.doi.org/10.1073/pnas.0405266101; http://www.ncbi.nlm.nih.gov/pubmed/15353589; https://pnas.org/doi/full/10.1073/pnas.0405266101; https://dx.doi.org/10.1073/pnas.0405266101; https://www.pnas.org/content/101/39/14186
Proceedings of the National Academy of Sciences
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