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home:publications:proal_autoimmunity_reviews_2009 [11.11.2009] – paulalbert | home:publications:proal_autoimmunity_reviews_2009 [11.11.2009] – paulalbert | ||
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**See also:** [[http:// | **See also:** [[http:// | ||
**Notes:** Paper based on [[home: | **Notes:** Paper based on [[home: | ||
- | **Faculty of 1000 mention: | + | |
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+ | ===== Abstract ===== | ||
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+ | Studies of autoimmune disease have focused on the characteristics of the identifiable antibodies. But as our knowledge of the genes associated with the disease states expands, we understand that humans must be viewed as superorganisms in which a plethora of bacterial genomes – a metagenome - work in tandem with our own. The NIH has estimated that 90% of the cells in Homo sapiens are microbial and not human in origin. Some of these microbes create metabolites that interfere with the expression of genes associated with autoimmune disease. Thus, we must re-examine how human gene transcription is affected by the plethora of microbial metabolites. We can no longer assume that antibodies generated in autoimmune disease are created solely as autoantibodies to human DNA. Evidence is now emerging that the human microbiota accumulates during a lifetime, and a variety of persistence mechanisms are coming to light. In one model, obstruction of VDR nuclear-receptor-transcription prevents the innate immune system from making key antimicrobials, | ||
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+ | =====Appraisal by Faculty of 1000===== | ||
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+ | Dr. Steven Witkin writing in the prestigious literary awareness tool, [[http:// | ||
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colonization account for individual variations in gene expression. Lastly, the | colonization account for individual variations in gene expression. Lastly, the | ||
potential pivotal role of endogenous microbial genomes on the induction and | potential pivotal role of endogenous microbial genomes on the induction and | ||
- | persistence of autoimmune disease is emphasized. | + | persistence of autoimmune disease is emphasized. |
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+ | //**Dr. Steven Witkin,** Weill Cornell Medical College// | ||
</ | </ | ||
- | ===== Abstract ===== | ||
- | Studies of autoimmune disease have focused on the characteristics of the identifiable antibodies. But as our knowledge of the genes associated with the disease states expands, we understand that humans must be viewed as superorganisms in which a plethora of bacterial genomes – a metagenome - work in tandem with our own. The NIH has estimated that 90% of the cells in Homo sapiens are microbial and not human in origin. Some of these microbes create metabolites that interfere with the expression of genes associated with autoimmune disease. Thus, we must re-examine how human gene transcription is affected by the plethora of microbial metabolites. We can no longer assume that antibodies generated in autoimmune disease are created solely as autoantibodies to human DNA. Evidence is now emerging that the human microbiota accumulates during a lifetime, and a variety of persistence mechanisms are coming to light. In one model, obstruction of VDR nuclear-receptor-transcription prevents the innate immune system from making key antimicrobials, | ||
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