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home:publications:proal_autoimmunity_2010 [06.15.2010] – marysue | home:publications:proal_autoimmunity_2010 [06.15.2010] – marysue | ||
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====#8 Nuclear receptors down regulated upon infection==== | ====#8 Nuclear receptors down regulated upon infection==== | ||
- | Take, for example, the Vitamin D Receptor or VDR - a type 1 nuclear receptor. Well, it turns out that viruses like Epstein-Barr Virus and bacteria like // | + | Take, for example, the Vitamin D Receptor or VDR - it' |
====#9 The Vitamin D Receptor (VDR)==== | ====#9 The Vitamin D Receptor (VDR)==== | ||
- | Why the VDR? Well, colloquially speaking, the VDR serves as a " | + | So, basically - you might ask, why the VDR? Well, colloquially speaking, the VDR serves as a " |
====#10 HIV and Borrelia burgdorferi==== | ====#10 HIV and Borrelia burgdorferi==== | ||
- | Note that HIV persists in the same fashion. It completely overtakes the VDR in order to transcribe its own genome.(({{pubmed> | + | And note that HIV persists in the same fashion. It completely overtakes the VDR in order to transcribe its own genome.(({{pubmed> |
- | This is such a logical survival mechanism on the part of these microbes that it is almost certain other less well-studied microbes have also evolved to slow VDR activity, or the activity of other receptors involved in controlling the immune response. | + | So - this is such a logical survival mechanism on the part of these microbes that it' |
====#11 Successive infection==== | ====#11 Successive infection==== | ||
- | Well, these persistence mechanisms result in a snowball effect. When the immune system slows, and a person acquires one pathogen, then it becomes easier to acquire another pathogen. | + | Well, these persistence mechanisms result in a snowball effect. When the immune system slows, and a person acquires one pathogen, then it becomes easier |
In the context of successive infection, an inflammatory disease state appears to result from the combined pathogenicity of the sum of microbes that any one person accumulates over the course of a lifetime. As human genes are upregulated or downregulated by components of these microbes, the human body shifts further and further away from its natural state of homeostasis. | In the context of successive infection, an inflammatory disease state appears to result from the combined pathogenicity of the sum of microbes that any one person accumulates over the course of a lifetime. As human genes are upregulated or downregulated by components of these microbes, the human body shifts further and further away from its natural state of homeostasis. | ||
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====#12 Epstein-Barr Virus (EBV)==== | ====#12 Epstein-Barr Virus (EBV)==== | ||
- | So, for example, over the past years, Epstein-Barr Virus has been detected in so many different proportions in so many disease states. | + | So, for example, over the past years, Epstein-Barr Virus has been detected in so many different proportions in so many disease states. |
====#13 Pathogens, aka " | ====#13 Pathogens, aka " | ||
- | With this in mind, a "one microbe/one disease" | + | With this in mind, a "one microbe/one disease" |
====#14 Co-morbidities among inflammatory diagnoses==== | ====#14 Co-morbidities among inflammatory diagnoses==== | ||
- | Well, it may also not be by accident that the uniqueness with which a patients' | + | Well, it may also not be by accident that the uniqueness with which a patients' |
====#15 Select bacterial genera detected in commonly smoked cigarettes==== | ====#15 Select bacterial genera detected in commonly smoked cigarettes==== | ||
- | So, where do we pick up these pathogens? They' | + | So, where do we pick up these pathogens? They' |
- | Finally, and I want to stress this, the model of successive infection has great implications for the way autoimmune disease should be treated. If microbes - both bacterial and viral - are driving the autoimmune disease state, then treatments that suppress the immune response can best succeed | + | Finally, and I want to stress this, the model of successive infection has great implications for the way autoimmune disease should be treated. If microbes - both bacterial and viral - are driving the autoimmune disease state, then treatments that suppress the immune response can at best succeed |
+ | |||
+ | Well, this being said, I work with the non-profit Autoimmunity Research Foundation and we, over the last six years have been working with a treatment for autoimmune disease that stimulates rather than suppresses the immune response in autoimmune disease. And, key to the treatment is the use of a VDR agonist which turns on - returns on - those components of the innate immune system that I described before that were so important. | ||
- | Well, this being said, I work with the non-profit Autoimmunity Research Foundation and we, over the last six years have been working with a treatment for autoimmune disease that stimulates rather than suppresses the immune response in autoimmune disease. And, key to the treatment is the use of a VDR agonist which turns on - returns on - those key components of the innate immune system that I described before that were so important. | ||
====#16 " | ====#16 " | ||