IL-23 Is Critical in the Induction but Not in the Effector Phase of Experimental Autoimmune Encephalomyelitis

By P. Thakker, M. Leach, W. Kuang, Stephen E. Benoit, J. Leonard, S. Marušić. 2007

189 citations recorded by the source corpus.

Subfields: Immunology, Oncology, Pathology and Forensic Medicine

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. K. Honda
2. J. Wing
3. K. Mills
4. Shimon Sakaguchi
5. G. Eberl
6. C. A. Dinarello
7. Alexander Y. Rudensky
8. E. Shevach

In Oncology

1. K. Honda
2. Shimon Sakaguchi

In Pathology and Forensic Medicine

1. C. A. Dinarello

Citations in the corpus

• Interleukin-1 and IL-23 induce innate IL-17 production from gammadelta T cells, amplifying Th17 responses and autoimmunity. (2009, background): “However, studies in an EAE model, involving adoptive transfer of T cells into Il23a / mice, showed that IL-23 played a critical role in the development but not in the effector function of encephalitogenic T cells (Thakker et al., 2007).”
• The microbiota regulates type 2 immunity through RORγt+ T cells (2015, methodology): “2 Materials and Methods Mice Foxp3 mice (43) were crossed to Rorc(γt) mice (15) and maintained on a C57BL/6 background, as were Cd11c x Rosa26 (ΔDC) mice (44), IL-2-deficient (45), IL-10deficient (46), IL-6-deficient (47), Il23a-deficient (48), Nod1/Nod2- and Myd88/Trifdouble deficient mice, Il10 (2”