IL-23 and IL-17 in the establishment of protective pulmonary CD4+ T cell responses after vaccination and during Mycobacterium tuberculosis challenge

By S. Khader, G. Bell, J. Pearl, Jeffrey J. Fountain, J. Rangel-Moreno, Garth E Cilley, F. Shen, Sheri M. Eaton, S. Gaffen, S. Swain and 4 more. Nature Immunology, 2007

1,498 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology, Infectious Diseases

View Paper: https://www.semanticscholar.org/paper/847c954547852db285edfa6d0dfc3d21cf8c5a69

How researchers see this paper

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In Epidemiology

1. A. O’Garra
2. F. Sallusto
3. R. Wilkinson
4. A. Lanzavecchia
5. M. Berry
6. Finlay W Mcnab
7. Paul S. Redford
8. C. Bloom

In Immunology

1. F. Sallusto
2. A. Lanzavecchia
3. D. Cua
4. C. Tato
5. Hua Yu
6. M. McGeachy
7. A. O’Garra
8. B. Engelhardt

In Infectious Diseases

1. A. O’Garra
2. R. Wilkinson
3. M. Berry
4. Finlay W Mcnab
5. Paul S. Redford
6. C. Bloom

Citations in the corpus

• Th17 cell differentiation: the long and winding road. (2008, positive): “Prat and colleagues elegantly demonstrated that receptors for IL-17 and IL-22 are present on inflamed endothelium in MS lesions and that these cytokines may potentiate migration of inflammatory T cells across the blood-brain barrier ( Kebir et al., 2007 ).”
• The immune response in tuberculosis. (2013, background): “Following vaccination with a mycobacterial peptide, IL-17 is required for the accelerated recruitment of IFN-γ-producing cells to the lung, as a result of increased concentrations of the chemokines CXCL9, 10, and 11, which recruit cells to sites of inflammation (287).”
• Innate IL-17-producing cells: the sentinels of the immune system (2010, background): “Furthermore, there is increasing evidence that early IL-17 production may also influence the subsequent effector CD4 + T cell response, particularly T H 1 cell”