Supported by the Italian Ministry of Research (PRIN), Istituto Pasteur – Fondazione Cenci Bolognetti, La Sapienza University (Ateneo Federato).
NKG2D/Ligand dysregulation and functional alteration of innate immunity cell populations in pediatric IBD†
Version of Record online: 31 JAN 2012
Copyright © 2012 Crohn's & Colitis Foundation of America, Inc.
Inflammatory Bowel Diseases
Volume 18, Issue 10, pages 1910–1922, October 2012
How to Cite
La Scaleia, R., Stoppacciaro, A., Oliva, S., Morrone, S., Di Nardo, G., Santoni, A., Cucchiara, S. and Palmieri, G. (2012), NKG2D/Ligand dysregulation and functional alteration of innate immunity cell populations in pediatric IBD. Inflamm Bowel Dis, 18: 1910–1922. doi: 10.1002/ibd.22899
- Issue online: 13 SEP 2012
- Version of Record online: 31 JAN 2012
- Manuscript Accepted: 3 JAN 2012
- Manuscript Received: 13 NOV 2011
Additional Supporting Information may be found in the online version of this article.
|IBD_22899_sm_SuppFig1.tif||2107K||Supporting Information Figure 1. Phenotypic characterization of peripheral blood NKR+ T subset in pediatric controls and IBD patients. Panel A: the frequency of CD3+CD56+ T cell subsets was evaluated in IBD patients (black symbols) and age-matched control individuals (white symbols). Panel B: the percentage of CD4+CD3+CD56+ T cells was evaluated in controls and active (IBDa, black symbols) or quiescent (IBDr, grey symbols) (left graph), and in CD (black symbols) or UC (gray symbols) (right graph) patients. Bars show median and interquartile range. *P< .05. Panel C: representative dot-plot analysis of CD4 and CD8 expression on CD3+CD56+ gated cells in a control (C), an active (IBDa), and a quiescent (IBDr) IBD patient. Numbers represent the percentage of CD4+ NKR+ T cells.|
|IBD_22899_sm_SuppFig2.tif||818K||Supporting Information Figure 2. NKG2D is functionally competent on fresh circulating NKR+ T cells from pediatric IBD patients but not age-matched controls. The frequency of polyfunctional (IFN γ+ CD107a+) cells obtained from pediatric IBD patients (black symbols) or age-matched controls (white symbols) was measured on CD3+CD56+ gated peripheral blood T lymphocytes, which were left unstimulated (NT), or upon stimulation with anti-CD3 + anti-CD28 (3/28), or with anti-CD3 + anti-CD28 + anti-NKG2D (+NKG2D) mAb. Peripheral blood mononuclear cells were either stimulated ex vivo (Panel A, fresh), or upon 18-h preincubation with 100 U/ml IL-2 (Panel B, IL-2 activated). Symbols represents mean + SEM, and are representative of 5 controls, 12 CD and 4 UC patients. For clarity, only the significativity of the comparison between anti-CD3/anti-CD28/anti-NKG2D and anti-CD3/anti-CD28-treated samples is reported. *P< .05; **P< .005.|
|IBD_22899_sm_SuppTab1.doc||40K||Supporting Information Table 1. Percentage of NKG2D+ cells in PBMC subsets of pediatric control and IBD patients|
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