Macrophage effector responses of horses are influenced by expression of CD154.
Abstract: Reactive intermediates contribute to innate immunity by providing phagocytes with a mechanism of defense against bacteria, viruses and parasites. To better characterize the role of CD154 in the production of reactive intermediates, we cloned and expressed recombinant equine CD154 (reqCD154) in Chinese Hamster Ovary (CHO). In co-culture experiments, CHO cells ectopically expressing reqCD154 elicited superoxide production in monocyte-derived macrophages (MDM). Collectively, our results indicate that regulation of CD154 expression plays a role in innate host defenses.
Copyright © 2016 Elsevier B.V. All rights reserved.
Publication Date: 2016-08-26 PubMed ID: 27692094PubMed Central: PMC7043372DOI: 10.1016/j.vetimm.2016.08.001Google Scholar: Lookup
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Summary
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This research article discusses the role of CD154 in stimulating the production of reactive intermediates by macrophages, using cells genetically manipulated to express the equine version of CD154 as a model.
Overview of Research
- The research paper delves into the study of the CD154 protein, which is found on the surface of activated T cells, and its role in producing reactive intermediates. Reactive intermediates are short-lived molecules that play a crucial role in the immune response, acting as a defense mechanism against various harmful organisms such as bacteria, viruses, and parasites.
- Using the technique of genetic cloning, the researchers were able to produce a recombinant form of equine CD154 (reqCD154), which means they essentially created a copy of the CD154 protein that is typically found in horses.
- The researchers used Chinese Hamster Ovary (CHO) cells as a tool for expression of the cloned eqCD154. CHO cells are commonly used in scientific research for protein production due to their rapid growth and the ease with which they can be genetically manipulated.
The Role of CD154 and Reactive Intermediates
- By co-culturing the CHO cells expressing the cloned equine CD154 with monocyte-derived macrophages (MDM), the researchers observed an increase in the production of a type of reactive intermediate known as superoxide.
- Superoxide is a reactive oxygen species that is often produced by phagocytic cells like macrophages, which are a type of white blood cell, as part of the inflammatory response. This suggests that the expression of CD154 plays a significant role in modulating the defensive response of macrophages.
- Based on their results, the researchers concluded that the regulation of CD154 expression has an impact on innate host defenses. Understanding the regulation of CD154 could potentially yield new insights and strategies in disease prevention and therapy.
Cite This Article
APA
Sponseller BA, Clark SK, Gilbertie J, Wong DM, Hepworth K, Wiechert S, Chandramani P, Sponseller BT, Alcott CJ, Bellaire B, Petersen AC, Jones DE.
(2016).
Macrophage effector responses of horses are influenced by expression of CD154.
Vet Immunol Immunopathol, 180, 40-44.
https://doi.org/10.1016/j.vetimm.2016.08.001 Publication
Researcher Affiliations
- Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, United States; Department of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, United States. Electronic address: baspon@iastate.edu.
- Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, United States. Electronic address: sclark@iastate.edu.
- Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, United States. Electronic address: skkyy1329@gmail.com.
- Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, United States. Electronic address: dwong@iastate.edu.
- Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, United States. Electronic address: katelhepworth@gmail.com.
- Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, United States. Electronic address: wiechert@iastate.edu.
- Department of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, United States. Electronic address: prashanth.chandramani@gmail.com.
- Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, United States. Electronic address: beatrice@iastate.edu.
- Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, United States. Electronic address: cjalcott@iastate.edu.
- Department of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, United States. Electronic address: bbella@iastate.edu.
- Department of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, United States. Electronic address: andyp@iastate.edu.
- Department of Veterinary Pathology, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, United States. Electronic address: jonesdou@iastate.edu.
MeSH Terms
- Animals
- CD40 Antigens / physiology
- CD40 Ligand / genetics
- CD40 Ligand / physiology
- CHO Cells
- Coculture Techniques
- Cricetinae
- Cricetulus
- Horses / immunology
- Macrophages / immunology
- Superoxides / metabolism
Grant Funding
- R15 HL103488 / NHLBI NIH HHS
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Citations
This article has been cited 2 times.- Schnabel CL, Fletemeyer B, Lübke S, Marti E, Wagner B, Alber G. CD154 Expression Indicates T Cell Activation Following Tetanus Toxoid Vaccination of Horses. Front Immunol 2022;13:805026.
- Phelps DW, Fletcher AA, Rodriguez-Nunez I, Balik-Meisner MR, Tokarz DA, Reif DM, Germolec DR, Yoder JA. In vivo assessment of respiratory burst inhibition by xenobiotic exposure using larval zebrafish. J Immunotoxicol 2020 Dec;17(1):94-104.
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