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Differentially induced expression of C-type lectins in activated lymphocytes
W Eichler1, P Ruschpler, M Wobus
1Faculty of Biosciences, Pharmaceutics and Psychology, University of Leipzig, Talstrasse 33, D-04103 Leipzig, Germany. eichwolf@uni-leipzig.de
Journal of Cellular Biochemistry. Supplement
|July 17, 2001
Summary
This study examines C-type lectin expression in activated lymphocytes, finding CD69, AICL, and LLT1 levels increase, while CD94 expression is protein synthesis-dependent. These distinct regulation mechanisms highlight differences in C-type lectin control.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- The human NK gene complex encodes C-type lectins crucial for lymphocyte function.
- These include CD69, AICL, LLT1, CD161/NKR-P1A, CD94, and NKG-2 molecules.
- These molecules regulate natural killer (NK) cells and other lymphocytes.
Purpose of the Study:
- To investigate C-type lectin expression during early lymphocyte activation.
- To determine the influence of de novo protein synthesis on activation-dependent C-type lectin expression.
Main Methods:
- Peripheral blood lymphocytes were stimulated with PMA.
- Cells were cultured with cycloheximide (CHX) to inhibit protein synthesis.
- mRNA levels were analyzed using semi-quantitative reverse transcription-polymerase chain reaction.
Main Results:
- CD69, AICL, and LLT1 mRNA levels were upregulated upon activation.
- CD69 showed superinduction by CHX, indicating transcriptional and post-transcriptional regulation.
- AICL, LLT1, and CD161/NKR-P1A mRNA were overexpressed with CHX treatment.
- CD94 mRNA expression was blocked by CHX, indicating dependence on new protein synthesis.
- Distinct regulatory mechanisms were identified for CD69, AICL, LLT1 versus CD161/NKR-P1A, CD94.
Conclusions:
- Early activation of lymphocytes involves differential regulation of C-type lectin gene expression.
- Mechanisms controlling CD69, AICL, and LLT1 upregulation differ from those of CD161/NKR-P1A and CD94.
- CD94 expression is dependent on ongoing protein synthesis during activation.