Related Experiment Video
Updated: Jul 3, 2026
Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
Published on: June 22, 2016
Inhibition of lymphocyte CD3 expression by Chlamydophila pneumoniae infection
Hiroyuki Yamaguchi1, Junji Matsuo, Shigehiro Sugimoto
1Laboratory of Molecular Microbiology, Department of Bioinformatics, Graduate School of Medicine, Osaka University, 1-7 Yamadaoka, Suita, Osaka 565-0871, Japan. hiroyuki@med.hokudai.ac.jp
Insights
Chlamydophila pneumoniae infection decreases CD3 expression on human lymphocytes. This effect is mediated by prostaglandin E2 (PGE2) and can be blocked by specific inhibitors, suggesting a novel mechanism in chronic inflammatory diseases.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Lymphocytes are key immune cells in atherosclerosis development.
- Chlamydophila pneumoniae infection is linked to chronic inflammatory diseases.
- Understanding lymphocyte-C. pneumoniae interactions is crucial for disease pathogenesis.
Purpose of the Study:
- To investigate the effect of C. pneumoniae infection on CD3 expression in human lymphocytes.
- To elucidate the role of prostaglandin E2 (PGE2) in this interaction.
Main Methods:
- Infection of human lymphocyte Molt-4 cells and primary lymphocytes with C. pneumoniae.
- Quantification of CD3 expression levels.
- Treatment with cyclooxygenase-2 inhibitor (NS-398) and EP4 receptor antagonist (AH-23848).
- Measurement of PGE2 production using competitive ELISA.
Main Results:
- C. pneumoniae infection significantly decreased CD3 expression on Molt-4 cells and primary lymphocytes.
- Heat-killed C. pneumoniae or cell lysates did not affect CD3 expression.
- Inhibition of CD3 expression was abolished by NS-398 and AH-23848.
- C. pneumoniae infection enhanced PGE2 production in lymphocyte cultures.
Conclusions:
- C. pneumoniae infection induces a decrease in lymphocyte CD3 expression.
- This downregulation is likely mediated by PGE2 production.
- Targeting the PGE2 pathway may offer therapeutic strategies for C. pneumoniae-associated inflammatory diseases.
Abstract:
Since lymphocytes are a major immune cell besides macrophages in the development of atherosclerosis, interaction between lymphocytes and Chlamydophila pneumoniae may contribute to the pathogenesis of chronic inflammatory diseases associated with C. pneumoniae. In this regard, we examined a possible alteration of CD3 expression of human lymphocyte Molt-4 cells by C. pneumoniae infection. The expression levels of CD3 molecules of lymphocyte Molt-4 cells were significantly decreased by C. pneumoniae infection. In contrast, heat-killed C. pneumoniae as well as mock (cell lysates) did not cause any alteration of CD3 expression of the cells. Treatment of the infected cells with NS-398 (cyclo-oxyganase-2 inhibitor) or AH-23848 (EP(4) prostanoid receptor antagonist) abolished the inhibition of CD3 expression. The enhanced prostaglandin E(2) (PGE(2)) productions in the culture supernatants of infected cells were confirmed by competitive enzyme-immunosorbent assay (ELISA). C. pneumoniae infection of enriched lymphocytes from human peripheral blood mononuclear cells also induced a decrease of CD3 expression. Thus, C. pneumoniae infection of lymphocytes induces a decrease of CD3 expression mediated by possibly PGE(2) production.
More Related Videos
09:26In Vitro Assay to Evaluate the Impact of Immunoregulatory Pathways on HIV-specific CD4 T Cell Effector Function
Published on: October 15, 2013
08:11Assessing the Innate Sensing of HIV-1 Infected CD4+ T Cells by Plasmacytoid Dendritic Cells Using an Ex vivo Co-culture System.
Published on: September 1, 2015
Related Concept Videos
01:29Bacterial Phylum Chlamydiae
01:25Immunodeficiency Diseases
There are three main causes of immunodeficiency disorders...