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Autologous Hematopoietic Stem Cell Transplantation for Crohn’s Disease
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Robert M. Craig, Richard K. Burt
The occurrence of a Th1 cytokine imbalance in Crohn’s is probably multi-factorial involving multiple environmental stimuli interacting with genetic predisposition resulting in a skewed but sometimes reversible cytokine imbalance. It is anticipated, but unproven, that HSCT will restore the normal cytokine balance. NOD2 is a Crohn’s associated gene contributing to, but not sufficient to cause, disease.32 NOD (nucleotide-binding oligomerization domain) proteins are involved in programmed cell death and innate immune responses.33 NOD2 is restricted to monocytes and activates NF-kappaB in response to bacterial products. Premature truncation of the NOD2 gene confers disease susceptibility in a subset of Crohn’s patients.34 Besides cytokine imbalance, and T cell immune responses to Saccharomyces cerevisiae and enteric bacteria, NOD2 gene polymorphisms which probably contribute to the immune deviation seen in Crohns, could be analyzed in patients undergoing HSCT.
Inflammatory bowel disease: why this provides a useful example of the evolving science of nutrigenomics
Published in Journal of the Royal Society of New Zealand, 2020
Familial aspects of IBD were recognised and reported as early as the 1970s (Singer et al. 1971). In their 1994 review, Satsangi et al. (1994) reported the use of genome scanning techniques using microsatellite markers, to implicate specific areas of chromosomes linked to disease, while association studies of specific genes or gene complexes, such as the human leukocyte antigen (HLA) gene complex, which encodes the major histocompatibility complex (MHC) proteins, were also linked to the risk of this disease in humans. HLA or cytokine genes were considered in early IBD studies to aid in mechanistic understandings, and this association was reinforced by subsequent findings (Satsangi et al. 1996). The possible involvement of the X chromosome was also suggested at an early stage, since there was a somewhat higher number of reported cases in women than in men (Vermeire et al. 2001). The situation appeared considerably more complex than a single gene disorder, and by the year 2000, Orchard and co-workers estimated the involvement of at least somewhere between 10 and 20 genes in disease susceptibility (Orchard et al. 2000). One gene that appeared of considerable importance in these early studies was the nucleotide-binding oligomerization domain-containing protein 2 (NOD2) gene (Hugot et al. 2001). This gene, also known as caspase recruitment domain-containing protein 15 (CARD15) or inflammatory bowel disease protein 1 (IBD1), is a protein that is encoded by the NOD2 gene, located on chromosome 16 in humans.