Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells

By E. Bettelli, Y. Carrier, Wenda Gao, T. Korn, T. Strom, M. Oukka, Howard L. Weiner, V. Kuchroo. Nature, 2006

7,364 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/73ba8dd9a638315f85a07eee116ab06b75f38f0c

How researchers see this paper

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

In Immunology

Citations in the corpus

Differentiation of Effector CD4 T Cell Populations (2010, neutral): “For example, IL-23 receptors appear not to be expressed until after the naive cell has partially completed its differentiation to becoming a Th17 cell, and consequently IL-23 plays little part in the initial determination of Th17 differentiation (21, 41, 43).”
Late Developmental Plasticity in the T Helper 17 Lineage (2009, background): “Th17 cells differentiate from naive CD4 T cell precursors in response to transforming growth factor (TGF)-b and IL-6; the Th1 lineage-associated factors signal transducer and activator of transcription (STAT)1, T-bet, and STAT4, as well as the Th2 factors STAT6 and GATA3, are dispensable for Th17 di”
Specific microbiota direct the differentiation of Th17 cells in the mucosa of the small intestine (2008, neutral): “Because Th17 and Treg cells are thought to be closely related in their differentiation programs (Bettelli et al., 2006; Zhou et al., 2008), we examined the frequency of Foxp3 cells in the SI LP of germ-free mice by flow cytometry (Figures 4C and S7).”
HIF1α–dependent glycolytic pathway orchestrates a metabolic checkpoint for the differentiation of TH17 and Treg cells (2011, background): “This is in agreement with the notion that the dichotomy of TH17 and Treg cell is dependent on an inflammatory environment, especially the concentration of IL-6 (Bettelli et al., 2006).”
Expanded Double Negative T Cells in Patients with Systemic Lupus Erythematosus Produce IL-17 and Infiltrate the Kidneys (2008, background): “Low IL-2 production (21), accompanied by high IL-6 secretion by APCs (27), could result in a skewed naive T cell differentiation, favoring Th17 over regulatory T cell production (28, 29).”
Peripheral CD4 T cell differentiation regulated by networks of cytokines and transcription factors (2010, background): “TGFb promotes the development of Th17 (8–10) or Treg cells (9, 14), but it suppresses Th1 and Th2 cell differentiation (27–29).”
Th17 cells express interleukin-10 receptor and are controlled by Foxp3− and Foxp3+ regulatory CD4+ T cells in an interleukin-10 dependent manner (2011, background): “The cytokines responsible for the differentiation of Th17 cells are already well defined; IL-6, TGF-b, and IL-1b are known to drive Th17 cell differentiation (Bettelli et al., 2006; Mangan et al., 2006; Sutton et al., 2006; Veldhoen et al., 2006).”