Association between innate response to gliadin and activation of pathogenic T cells in coeliac disease.

By L. Maiuri, C. Ciacci, I. Ricciardelli, L. Vacca, V. Raia, S. Auricchio, Jean Picard, Mohamed Osman, S. Quaratino, M. Londei. The Lancet, 2003

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Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor 4 (2012, methodology): “However, additional modulating factors, including cereal stimulants of innate immunity, were suspected, but their clear identity and signaling receptors remained elusive (Maiuri et al., 2003; Nikulina et al., 2004; Cinova et al., 2007).”
Coordinated induction by IL15 of a TCR-independent NKG2D signaling pathway converts CTL into lymphokine-activated killer cells in celiac disease. (2004, background): “At the time of study, 35 had active celiac disease with (Maiuri et al., 2003), perhaps initiating the deleterious partial villous atrophy whereas 25 had been under strict gluten-free series of events leading to uncontrolled destruction of IEC.”