http://gut.bmj.com/content/52/10/1522.fullAbstract
Dendritic cells are antigen presenting cells that are likely to be pivotal in the balance between tolerance and active immunity to commensal microorganisms that is fundamental to inflammatory conditions, including Crohn’s disease and ulcerative colitis. Interactions between dendritic cells and microbial products are discussed and how they contribute to regulation of immune responses. The concept that interactions between dendritic cells and commensal organisms may be responsible for maintaining intestinal immune homeostasis is also explored.
I found a brand-new article about Dermatomyositis which questions the pathophysiology of the disease, and points to the action of dendritic cells.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3482801/DM has traditionally been viewed as a humorally mediated vasculopathic disease given the findings of autoantibodies and complement deposition in vessels.[13] The proposed mechanism has been that binding of antibodies targeting the endothelium of the endomysial capillaries leads to activation of the complement system with subsequent MAC deposition. This in turn may lead to endothelial swelling, capillary necrosis, perivascular inflammation, and muscle ischemia. Relative hypoperfusion of the perifascicular regions is thought to explain the findings of atrophy in this region on muscle biopsy. This model of DM pathogenesis, however, is unproven.[14] Certain limitations to this model include the absence of an identified pathogenic antibody against an endothelial antigen, and the unclear relationship between capillary injury and perifascicular atrophy, since the perifascicular area has not been shown to be specifically vulnerable to ischemia.[14]
Data using gene expression microarrays have demonstrated upregulation of interferon signaling in the muscle, blood, and skin of DM patients.[15] In muscle, almost 90% of the highly expressed gene transcripts in DM compared with controls belong to genes that are induced by the type 1 interferons.[15] In addition, the finding that plasmacytoid dendritic cells are present in skin and muscle of DM patients, implicates these cells as potential sources of the interferons. Based on these findings, Greenberg has proposed a revised model of DM wherein endothelial cells and myofibers may be injured by the chronic overproduction intracellularly of one or more interferon α/β inducible proteins.[15] It has been proposed that interferons produced by plasmacytoid dendritic cells, which are typically found in higher concentration in perimysial regions, may contribute to perifascicular atrophy. What still remains unclear is what might be driving the transcription of interferon α/β inducible genes and whether viral DNA and RNA substrates could potentially be activating the plasmacytoid dendritic cells.
I'm not sure where this is all taking me, but hopefully somewhere. I've also read that some people with ADM respond favorably (and quickly!) to IVIG treatment without the need for steroids and other meds. The challenge will probably be finding insurers to cover IVIG as a first-line treatment.
Still digging...
