Citations 2
Predicting missing biomarker data in a longitudinal study of Alzheimer disease
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Neurology | April 5, 2012 | Volume: 78 | Issue: 18 | Pages: 1376-1382
Circulating and gut-resident human Th17 cells express CD161 and promote intestinal inflammation
Kleinschek, Melanie A., Boniface, Katia , Sadekova, Svetlana , Grein, Jeff, Murphy, Erin E., Turner, Scott, Raskin, Lisa A., Desai, Bela, Faubion, William A. , Malefyt, René de Waal , McClanahan, Terrill K., Kastelein, Robert A., Pierce, Robert Hamilton
Journal of Experimental Medicine | March 9, 2009 | Volume: 206 | Issue: 3 | Pages: 525-534
The C-type lectin-like receptor CD161, which has recently been described to promote T cell expansion, is expressed on a discrete subset of human CD4 T cells. The function of such cells, however, has remained elusive. We now demonstrate that CD161+ CD4 T cells comprise a circulating and gut-resident T helper 17 (Th17) cell population. During Crohn's disease (CD), these CD161+ cells display an activated Th17 phenotype, as indicated by increased expression of interleukin (IL)-17, IL-22, and IL-23 receptor. CD161+ CD4 T cells from CD patients readily produce IL-17 and interferon γ upon stimulation with IL-23, whereas, in healthy subjects, priming by additional inflammatory stimuli such as IL-1β was required to enable IL-23–induced cytokine release. Circulating CD161+ Th17 cells are imprinted for gut homing, as indicated by high levels of CC chemokine receptor 6 and integrin β7 expression. Supporting their colitogenic phenotype, CD161+ Th17 cells were found in increased numbers in the inflammatory infiltrate of CD lesions and induced expression of inflammatory mediators by intestinal cells. Our data identify CD161+ CD4 T cells as a resting Th17 pool that can be activated by IL-23 and mediate destructive tissue inflammation.