Genetic architecture of early pre-inflammatory stage transcription signatures of autoimmune diabetes in the pancreatic lymph nodes of the NOD mouse reveals significant gene enrichment on chromosomes 6 and 7.

摘要: Autoimmune diseases are characterized by the stimulation of an excessive immune response to self-tissues inner and/or outer organism factors. Common characteristics in their etiology include a complex genetic predisposition and environmental triggers as well implication major histocompatibility (MHC) locus on human chromosome 6p21. A restraint number non-MHC susceptibility genes, part component type 1 diabetes have been identified animal models, while complete spectrum genes involved remains unknown. We elaborate herein patterns chromosomal organization 162 differentially expressed pancreatic lymph nodes Non-Obese Diabetic mice, carefully selected early sub-phenotypic evaluation (presence or absence insulin autoantibodies). Chromosomal assignment these revealed non-random distribution five chromosomes (47%). Significant gene enrichment was observed particular for two chromosomes, 6 7. While subset coding secreted proteins showed significant both overall pool significantly enriched The significance this unexpected mouse genome is discussed light novel findings indicating that affecting common map recombination “hotspot” regions mammalian genomes. architecture transcripts specific stages autoimmune offers venues towards our understanding inheritance potentially pathological disease mechanisms.