Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2001:Suppl 36:201-8.
doi: 10.1002/jcb.1107.

Differentially induced expression of C-type lectins in activated lymphocytes

Affiliations

Differentially induced expression of C-type lectins in activated lymphocytes

W Eichler et al. J Cell Biochem Suppl. 2001.

Abstract

The human NK gene complex encodes for the leucocyte C-type lectins, CD69, AICL (activation-induced C-type lectin), LLT1 (lectin-like transcript), CD161/NKR-P1A, CD94, and for NKG-2 molecules. These gene products have been implicated in the regulation of the function of natural killer (NK) cells and other lymphocytes. In this study the expression of C-type lectins during the early activation of PMA-stimulated peripheral blood lymphocytes was examined. To investigate the influence of de novo protein synthesis on activation-dependent expression of C-type lectins, cells were cultured in presence of cycloheximide (CHX) and mRNA levels were analyzed by semi-quantitative reverse transcription-polymerase chain reaction. Upregulated levels of CD69, AICL, and LLT1, but less pronounced changes of CD161/NKR-P1A and CD94 mRNA were found at early time points of cellular activation. CD69 was superinduced by CHX at the nuclear precursor transcript and the mRNA level suggesting that regulation of transcriptional activity and mRNA stability contribute to extent of CD69 mRNA accumulation. CHX treatment resulted also in an overexpression of AICL, LLT1, and CD161/NKR-P1A mRNAs. Conversely, CHX blocked CD94 mRNA expression in PMA-stimulated cells, demonstrating that this process is dependent on new protein synthesis. Expression kinetics in context with susceptibility to CHX indicate that the mechanisms responsible for upregulated CD69, AICL, and LLT1 expression are distinct from those which control CD161/NKR-P1A or CD94 expression. J. Cell. Biochem. Suppl. 36: 201-208, 2001.

PubMed Disclaimer

Publication types

MeSH terms

LinkOut - more resources