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--- home:publications:proal_metagenomics_2010 [11.17.2010] – created paulalbert
+++ home:publications:proal_metagenomics_2010 [11.17.2010] – paulalbert
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 **Authors:**  Amy Proal, Paul Albert, Trevor Marshall PhD\\
 **Publication:** //Vitamin D: New Research//\\
-**Citation:**  Proal AD et al. Autoimmune disease and the human metagenome. //Metagenomics of the human body// 231-75(2010).\\
+**Citation:**  Proal AD //et al//. Autoimmune disease and the human metagenome. //Metagenomics of the human body// 231-75(2010).\\
 **See also:** [[http://Autoimmunityresearch.org/preprints/Proal_MHB_Chapter_preprint.pdf|Pre-print]]
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 ===== Abstract =====
-The prevailing theory of autoimmune disease, that the body creates autoantibodies that attack “self,” was developed during an era when culture-based methods vastly underestimated the number of microbes capable of persisting in and on Homo sapiens. Thanks to the advent of culture-independent tools, the human body is now known to harbor billions of microbes whose collective genomes work in concert with the human genome. Thus, the human genome can no longer be studied in isolation. Some of these microbes persist by slowing the activity of the VDR nuclear receptor, affecting the expression of endogenous antimicrobials and other key components of the innate immune system. It seems that bacteria that cause autoimmune disease accumulate over a lifetime, with individuals picking up pathogens with greater ease over time, as the immune response becomes increasingly compromised. Any one autoimmune disease is likely due to many different microbes within the metagenomic microbiota. This helps explain the high levels of comorbidity observed amongst patients with autoimmune conditions. What are commonly believed to be autoantibodies may instead be created in response to this metagenomic microbiota, when the adaptive immune system is forced to deal with disintegration of infected cells. Similarly, haplotypes associated with autoimmune conditions vary widely amongst individuals and populations. They are more suggestive of a regional infectious model rather than a model in which an illness is caused by inherited variation of HLA haplotypes.
+The prevailing theory of autoimmune disease, that the body creates autoantibodies that attack "self," was developed during an era when culture-based methods vastly underestimated the number of microbes capable of persisting in and on //Homo sapiens//. Thanks to the advent of culture-independent tools, the human body is now known to harbor billions of microbes whose collective genomes work in concert with the human genome. Thus, the human genome can no longer be studied in isolation. Some of these microbes persist by slowing the activity of the VDR nuclear receptor, affecting the expression of endogenous antimicrobials and other key components of the innate immune system. It seems that bacteria that cause autoimmune disease accumulate over a lifetime, with individuals picking up pathogens with greater ease over time, as the immune response becomes increasingly compromised. Any one autoimmune disease is likely due to many different microbes within the metagenomic microbiota. This helps explain the high levels of comorbidity observed amongst patients with autoimmune conditions. What are commonly believed to be autoantibodies may instead be created in response to this metagenomic microbiota, when the adaptive immune system is forced to deal with disintegration of infected cells. Similarly, haplotypes associated with autoimmune conditions vary widely amongst individuals and populations. They are more suggestive of a regional infectious model rather than a model in which an illness is caused by inherited variation of HLA haplotypes.
 {{tag>book_chapters Trevor_Marshall_PhD Amy_Proal Paul_Albert 2010}}

home/publications/proal_metagenomics_2010.txt · Last modified: 07.04.2022 by 127.0.0.1