1. The Th17 immune response in renal inflammation
Jan-Eric Turner, Hans-Joachim Paust, Oliver M. Steinmetz, Ulf Panzer 
Kidney International 
Volume 77, Issue 12, Pages (June 2010)
DOI: /ki
Copyright © 2010 International Society of Nephrology Terms and Conditions

2. Figure 1
Differentiation of CD4+ T-cell subsets. After the encounter of antigen and co-stimulatory molecules presented by antigen-presenting cells, naive CD4+ T cells can differentiate into different subpopulations. The lineage commitment of CD4+ T cells depends on the cytokine milieu accompanying the T-cell activation process in secondary lymphoid organs. The diverse T-helper cell subtypes show differential activation of transcriptional programs and are characterized by secretion of certain effector cytokines that enable them to provide protection against different classes of pathogens and to mediate autoimmunity. IFN-γ, interferon-γ; IL, interleukin; TGF-β, transforming growth factor-β; Th1, T-helper 1 cell; TNF-α, tumor necrosis factor-α.
Kidney International  , DOI: ( /ki )
Copyright © 2010 International Society of Nephrology Terms and Conditions

3. Figure 2
Current pathophysiological concept of Th17-mediated kidney injury. Infiltrating Th17 cells secrete IL-17 (also called IL-17A) that stimulates resident renal cells through the IL-17 receptor to produce chemokines and other inflammatory mediators. IL-17 induces expression of a specific chemokine pattern that primarily leads to the recruitment of neutrophils, but also includes monocyte- and Th1-cell-attracting chemokines. Furthermore, Th17 cells might facilitate the infiltration of additional Th17 cells directly by secretion of the chemokine CCL20 and indirectly by stimulating resident cells to produce CCL20. Recruitment of the other pro-inflammatory leukocyte subsets ultimately leads to the progression of immune-mediated kidney damage. IL, interleukin; Th1, T-helper 1 cell.
Kidney International  , DOI: ( /ki )
Copyright © 2010 International Society of Nephrology Terms and Conditions