Interleukins 1beta and 6 but not transforming growth factor-beta are essential for the differentiation of interleukin 17-producing human T helper cells.
By Eva Acosta-Rodriguez, G. Napolitani, A. Lanzavecchia, F. Sallusto. Nature Immunology, 2007
934 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/91d08bdbfb5de7093101857c60663281846b8a9a
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
- Andrew H. Miller
- L. Capuron
- Charles L Raison
- E. Haroon
- W. E. Paul
- J. O’Shea
- Jinfang Zhu
- P. Di Meglio
Citations in the corpus
- From Vaccines to Memory and Back (2010, unknown): “Likewise, in response to fungi or certain bacteria, DC and monocytes produce IL-1 β , IL-6 and IL-23 that drive differentiation of Th17 cells that through secretion of IL-17 and recruitment of neutrophils mediate protection against extracellular pathogens (Acosta-Rodriguez et al., 2007).”
- Human inflammatory dendritic cells induce Th17 cell differentiation. (2013, background): “…and IL-23 have been proposed to be involved in human Th17 cell polarization, but whether all these cytokines are essential has been controversial (Acosta-Rodriguez et al., 2007; Manel et al., 2008; Volpe Immunity 38, 336–348, February 21, 2013 ª2013 Elsevier Inc. 345 et al., 2008; Wilson et al.,…”
- The IL-23/Th17 axis in the immunopathogenesis of psoriasis. (2009, background): “…in the presence of toll-like receptor-activated monocytes (Evans et al., 2007) and also that proinflammatory cytokines, such as IL-1b and IL-6, alone or in combination with IL-23, were able to drive Th17 differentiation (Chen et al., 2007; Wilson et al., 2007; Acosta-Rodriguez et al., 2007a).”
- THE INTERLEUKIN-1 FAMILY: BACK TO THE FUTURE (2013, unknown): “Analysis of the differentiation of human naive T cells to Th17 cells originally revealed a key role of IL-1 (Acosta-Rodriguez et al., 2007; Annunziato et al., 2007).”
- Psychoneuroimmunology Meets Neuropsychopharmacology: Translational Implications of the Impact of Inflammation on Behavior (2012, background): “Th17 cells have been recently recognized as a distinct, highly pro-inflammatory T-cell subset that may have a fundamental pathophysiologic role in inflammatory disorders (Acosta-Rodriguez et al, 2007; Annunziato et al, 2007; Wilson et al, 2007; Tesmer et al, 2008; Damsker et al, 2010).”
- Retinoid-related orphan receptors (RORs): critical roles in development, immunity, circadian rhythm, and cellular metabolism (2009, background): “In contrast to IL-21, the induction of IL23R is greatly reduced in RORγ-deficient mice, suggesting that its expression is regulated by RORγt.”
- Modulation of Innate and Adaptive Immune Responses by Tofacitinib (CP-690,550) (2011, background): “In human cells, the requirement for TGF-b has been less clear, and lately the necessity for TGF-b in mouse has been called into question (49, 50).”
- Th17 cells in human disease (2008, background): “Several reports have found that human and mouse Th17 cells express the chemokine receptor CCR6, including memory cells from healthy peripheral blood and inflamed tissue as well as in vitro primed naı̈ve T cells (17, 19, 43, 54).”
- Peripheral CD4 T cell differentiation regulated by networks of cytokines and transcription factors (2010, background): “IL-1 and tumor necrosis factor-a (TNFa) are important inflammatory cytokines and IL-1 has been shown critical for the differentiation of Th17 cells, especially in humans (33, 42, 43).”
- Interleukin-17 production in central nervous system-infiltrating T cells and glial cells is associated with active disease in multiple sclerosis. (2008, background): “Transforming growth factor- is not needed for IL-17 production in human T cells and even inhibits IL-17 production, whereas IL-1 is a very effective and IL-6 a poor inducer of TH17 differentiation.(14,15) The role of human IL-23 in inducing IL-17-secreting cells is, however, unclear, because it has ”