A brief history of TH17, the first major revision in the TH1/TH2 hypothesis of T cell–mediated tissue damage
By L. Steinman. Nature Medicine, 2007
1,039 citations recorded by the source corpus.
Subfields: Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/9788044d1b2af4cd1284b49c5197a16354f7103a
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In Immunology
- F. Sallusto
- C. Iadecola
- A. Lanzavecchia
- J. Anrather
- C. Dong
- B. Engelhardt
- Antonio Uccelli
- Rafi Ahmed
In Oncology
Citations in the corpus
- TH17 cells in development: an updated view of their molecular identity and genetic programming (2008, background): “T H 17 cells are also increasingly being recognized as key players in autoimmune and inflammatory disease”
- Multiple Sclerosis (2018, background): “The precise role(s) of TH1 and TH17 CD4+ lymphocytes has yet to be determined with regard to MS, but it is likely that both types of lymphocytes play an important part.”
- The immunology of stroke: from mechanisms to translation (2011, background): “The recent identification of IL-17–secreting T cells as a crucial effector of the tissue damage in autoimmune diseases (T H 17 cells”
- Structure and signalling in the IL-17 receptor superfamily (2009, neutral): “In particular, deficiency in interleukin-12 (IL-12) (specifically, the IL-12p40 subunit of this heterodimeric cytokine), which drives the development of the T H 1 cell lineage, frequently failed to phenocopy deficiency in interferon-γ (IFNγ), the hallmark T H 1-type cytokin”
- 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): “Several lines of evidence indicate that T H -17 cells are involved in the onset and maintenance of EA”
- Differential glycosylation of TH1, TH2 and TH-17 effector cells selectively regulates susceptibility to cell death (2007, neutral): “dtd" [ ]> Activation of naive CD4 + T helper cells results in the development of functionally distinct effector T cells, which are responsible for orchestrating adaptive immune response”