Cutting Edge: Type I IFNs Provide a Third Signal to CD8 T Cells to Stimulate Clonal Expansion and Differentiation1

By Julie M. Curtsinger, Javier O. Valenzuela, P. Agarwal, Debra C. Lins, M. Mescher. Journal of Immunology, 2005

625 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Heterogeneity and cell-fate decisions in effector and memory CD8+ T cell differentiation during viral infection. (2007, background): “…in this process because IL-12 and IFN-g amounts can vary between different infections (Cousens et al., 1999), and likely candidates are type I IFNs (Curtsinger et al., 2005; Kolumam et al., 2005; Way et al., 2007), other IL-12 family members, or even Toll-like receptor ligands that act directly on…”
Type I interferon is selectively required by dendritic cells for immune rejection of tumors (2011, positive): “Treatment with IFN  /  in vitro pro longed the survival of activated T cells (Marrack et al., 1999) and augmented clonal expansion and effector differentiation of CD8 + T cells (Curtsinger et al., 2005) through cellintrinsic IFN  /  receptor signaling.”
Inflammatory Cytokines as a Third Signal for T Cell Activation (2010, positive): “At the same time, there is clearly a high degree of specificity; different cytokines are needed to provide signal 3 to CD8 versus CD4 T cells, and a large number of other proinflammatory cytokines have failed to exhibit signal 3-like activity for either CD8 [3] or CD4 [43,45] T cells.”