The homodimer interfaces of costimulatory receptors B7 and CD28 control their engagement and pro-inflammatory signaling
Abstract
The inflammatory response is indispensable for protective immunity, yet microbial pathogens often trigger an excessive response, ‘cytokine storm’, harmful to the host. Full T-cell activation requires interaction of costimulatory receptors B7-1(CD80) and B7-2(CD86) expressed on antigen-presenting cells with CD28 expressed on the T cells. We created short peptide mimetics of the homodimer interfaces of the B7 and CD28 receptors and examined their ability to attenuate B7/CD28 coligand engagement and signaling through CD28 for inflammatory cytokine induction in human immune cells, and to protect from lethal toxic shock in vivo.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Jun 28, 2023
- Source ID
- 10.1186/s12929-023-00941-3
Entities
People
- Andrey Popugailo
- Dalia Hillman
- Gila Arad
- Michal Levy
- Orli Turgeman
- Raymond Kaempfer
- Revital Levy
- Tomer Shpilka
- Ziv Rotfogel
Organizations
- Congressionally Directed Medical Research Programs
- Division of Intramural Research, National Institute of Allergy and Infectious Diseases