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Updated: Jul 6, 2026
11:48
Detection of Alternative Splicing During Epithelial-Mesenchymal Transition
Published on: October 9, 2014
A novel B7-2 (CD86) splice variant with a putative negative regulatory role
Efstathia K Kapsogeorgou1, Haralampos M Moutsopoulos, Menelaos N Manoussakis
1Laboratory of Cellular and Molecular Immunology, Department of Pathophysiology, School of Medicine, National University of Athens, Athens, Greece.
Journal of Immunology (Baltimore, Md. : 1950)
|March 7, 2008
Summary
A novel B7-2C transcript, lacking a key binding domain, is found in monocytes and salivary cells. It inhibits T cell costimulation by B7-2A, fine-tuning immune responses.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- B7-2 (CD86) molecules are crucial for regulating T cell responses.
- Understanding B7-2 regulation is key to controlling immune system activity.
Purpose of the Study:
- To describe a novel human B7-2 alternate transcript, B7-2C.
- To investigate the expression and function of B7-2C in immune and non-immune cells.
Main Methods:
- Characterization of the B7-2C transcript lacking exon 4.
- Detection of B7-2C mRNA and protein in various human cell types.
- Analysis of B7-2C function using Chinese hamster ovary (CHO) cell transfectants.
Main Results:
- B7-2C mRNA and protein were detected in human salivary gland epithelial cells and monocytes.
- B7-2C protein expression was down-regulated in monocytes upon activation.
- Cell surface B7-2C inhibited B7-2A-mediated T cell costimulation in a dose-dependent manner.
Conclusions:
- B7-2C is expressed in monocytes and non-immune cells like salivary gland epithelial cells.
- B7-2C acts as a negative regulator of B7-2A costimulatory signals.
- B7-2C may fine-tune T cell responses by modulating B7-2A clustering and function.
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