When disease-causing invaders like bacteria infect a human host, cells of various types swing into action, coordinating their activities to address the threat.
In new research appearing in this month's issue of the journal Nature Immunology, Roy Curtiss, director of the Center for Infectious Diseases and Vaccinology at the Biodesign Institute at Arizona State University, along with international collaborators, investigates the coordination of a particular type of immune response, involving the release of of IFN-λ a cell-signaling protein molecule known as a cytokine.
Molecules like IFN-λ have long been recognized as vital weapons in the immune system's arsenal against viral, bacterial and parasitic pathogens, as well as tumors. They are known as interferonsnamed for their ability to interfere with the functioning or replication of infectious agents. Communication between cells enabled by interferons can trigger the protective defenses of the immune system, which will attempt by various means to eradicate the infectious pathogen.
"The inception of this study was based on studies conducted in collaboration with the Richard Strugnell group at the University of Melbourne when it was shown that flagella produced by S. Typhimuriumand especially by a mutant generated by Shifeng Wang in our group, that hyper produced the flagellinwere superior in inducing a cascade in host cells leading to the production of NFκB," a protein complex that plays a key role in regulating the immune response to infection.
The cytokine IFN-λ is produced by a type of lymphocyte known as a memory CD8+ T cell. Memory T cells are a vital part of the adaptive immune system. Typically, they are activated and induced to proliferate when they come in contact with a specific antigen produced by the infectious agent and recognized by the T cell's antigen receptor. After their initial encounter with the unfamiliar invader, memory T cel
|Contact: Joseph Caspermeyer|
Arizona State University