Th17 cell differentiation: the long and winding road.

By M. McGeachy, D. Cua. Immunity, 2008

751 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/b760ce5f5fe460d31141ff00daf4d4af1159c60f

How researchers see this paper

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

In Immunology

1. R. Flavell
2. Ming O. Li
3. D. Cua
4. F. Sallusto
5. A. Lanzavecchia
6. J. O’Shea
7. C. Tato
8. C. Weaver

Citations in the corpus

• Interleukin-17-producing gammadelta T cells selectively expand in response to pathogen products and environmental signals. (2009, background): “The absence of IL-23 signals greatly affects the numbers of Th17 cells and results in the failure to recruit or activate these cells (McGeachy et al., 2009; McGeachy and Cua, 2008), and, similarly, IL-17-producing gd T cells were compromised in the absence of IL-23.”
• C-C chemokine receptor 6–regulated entry of TH-17 cells into the CNS through the choroid plexus is required for the initiation of EAE (2009, background): “Interleukin 17 (IL-17)-producing T cells (T H -17 cells) have been characterized in the mouse as a distinct lineage of CD4 + T cells that can differentiate from uncommitted naive T cell precursors under the aegis of the transcription factors RORγt and RORα and the polarizing cytokines transforming ”
• TGF-beta: a master of all T cell trades. (2008, positive): “Recent studies have expanded the Th1-Th2 cell paradigm with the addition of a newer helper T cell type, the Th17 cell (McGeachy and Cua, 2008).”
• Innate IL-17-producing cells: the sentinels of the immune system (2010, background): “The importance of T H 17 cells in immune responses and diseases has been reviewed in detail elsewher”
• Cytokine signaling modules in inflammatory responses. (2008, background): “The pathways for generating IL-22 are discussed in accompanying reviews in this issue by Ouyang et al. (2008), Li and Flavell (2008), and McGeachy and Cua (2008).”
• Epigenetic control of T-helper-cell differentiation (2009, background): “The transcription factors that are involved in T H 1- and T H 2-cell differentiation are not required for T H 17-cell differentiation and can antagonize this proces”
• Late Developmental Plasticity in the T Helper 17 Lineage (2009, background): “Prior to discovery of the Th17 lineage and a nonredundant role for IL-23 in several models of autoimmunity, immune pathogenesis in these models was ascribed to dysregulated Th1 responses (reviewed by McGeachy and Cua, 2008; Weaver et al., 2007).”
• Fate mapping of interleukin 17-producing T cells in inflammatory responses (2011, result): “that seemed to refute the idea of an important role for T H 17 cells in various autoimmune models, in contrast to earlier data highlighting their crucial importance in these model”
• Structure and signalling in the IL-17 receptor superfamily (2009, neutral): “The reader is referred to several excellent reviews on this topi”
• Interleukin-1 and IL-23 induce innate IL-17 production from gammadelta T cells, amplifying Th17 responses and autoimmunity. (2009, result): “These findings are consistent with the suggestions that IL-23 may be central to differentiation rather than expansion or survival of pathogenic Th17 cells (McGeachy and Cua, 2008; Wilson et al., 2007).”