Mechanisms of cooperation between antigenic and cytokine signals in CD8 T cell activation
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[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT REQUEST OF AUTHOR.] Our adaptive immune system is comprised of white-blood cells that distinguish self- (our own) from foreignproteins (DNA products) and are capable of establishing long-lived immunity against harmful microbes and cancer. One of the cellular subsets that mediate cellular immunity, or protection by distinction, called CD8 T cells, specifically kill only virally infected or cancerous cells. In order to do so, CD8 T cells must integrate signals from the environment that include sensing both small pieces of proteins presented by other immune cells and proteins produced by the inflammatory, or "early-warning", anti-microbial immune response. It is not clear how these two signals (antigen and inflammatory proteins) integrate to activate the cell-mediated immune response that leads to direct killing of infected cells. Answers to how these signals cooperate to activate the immune system, could provide insight into new therapies for caner, autoimmune diseases, and vaccinations. Here, we find specific conditions that lead to activation of CD8 T cells potentially able to respond to self-antigens important for auto-immunity and cancer. Specifically we found that the strength of signal through the receptor that recognizes small pieces of protein, influenced the T cell's ability to sense inflammatory proteins. Further, we found that signals from the inflammatory environment utilize the cell-membrane receptor used to sense small pieces of proteins from self or foreign sources. In an unexpected way response to inflammatory proteins required CD8 T cells to recognize, or sense, self-antigens.
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