GLIADIN PEPTIDE P31-43 ENHANCES IL15 ACTIVITY BY INTERFERING WITH ITS INTRACELLULAR TRAFFICKING
DIGESTIVE AND LIVER DISEASE
Authors: Santagata, S.; Zanzia, D.; Maglio, M.; Nanayakkara, M.; Lania, G.; Discepolo, V.; Kosova, R.; Ferrara, K.; Troiano, R.; Vitale, V.; Costa, S.; Troncone, R.; Auricchio, S.; Barone, M. V.
Abstract
Monocytes differentiated with IL-15 support Th17 and Th1 responses to wheat gliadin: Implications for celiac disease
CLINICAL IMMUNOLOGY
Authors: Harris, Kristina M.; Fasano, Alessio; Mann, Dean L.
Abstract
Interleukin (IL)-15 contributes to the immunopathogenesis of Celiac disease (CD). However, it is not clear how IL-15 affects APC that shape adaptive immune responses to the dietary antigen, gliadin. Using PBMC from healthy individuals, we show that monocytes differentiated with IL-15 (IL15-DC) produced IL-1 beta, IL-6, IL-15, IL-23, TNF alpha and CCL20 in response to pepsin-trypsin digested gliadin (PTG) and activated contact-dependent Th17 and Th1 responses from autologous CD4(+) T cells. Lower concentrations of IL-15 augmented IFN gamma responses to PTG in PBMC from CD patients compared to controls. Thus, IL-15 supports Th17 and Th1 responses to a dietary antigen that is normally well-tolerated in healthy individuals by generating IL15-DC These potentially pathogenic immune responses may result in CD patients and not healthy individuals as a consequence of IL-15 hypersensitivity. Therefore, genetic and/or environmental factors that control IL-15 expression and responsiveness in the intestine likely participate in the pathogenesis of CD. (C) 2010 Elsevier Inc. All rights reserved.
COA
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