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home:diseases:hiv_and_aids [02.17.2019] – [CD38] sallieqhome:diseases:hiv_and_aids [02.17.2019] – [at this time there are no AIDS patients on the Marshall Protocol] sallieq
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 Pathogens are able spread effectively in an immunocompromised environment. This means it's possible that AIDS patients pick up substantial pathogen loads. It is further possible that it is these Th1 pathogens, which kill patients. Viral co-infections (including Epstein-Barr virus, Human Herpes Virus 6, etc.) are found in all the diseases the Marshall Protocol treats, but the viruses are not believed to bethe proximate cause of disease.  Pathogens are able spread effectively in an immunocompromised environment. This means it's possible that AIDS patients pick up substantial pathogen loads. It is further possible that it is these Th1 pathogens, which kill patients. Viral co-infections (including Epstein-Barr virus, Human Herpes Virus 6, etc.) are found in all the diseases the Marshall Protocol treats, but the viruses are not believed to bethe proximate cause of disease. 
  
 +===== CD38 =====
  
  
-===== AIDS patients on the Marshall Protocol =====+CD38 plays a role in effective containment of mycobacteria within granulomata and polarization of Th1 immune responses against Mycobacterium avium. (({{pubmed>long:17533152}}))  
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 +Absence of CD38 rendered mice more susceptible to mycobacterial infection. This susceptibility seems to be due to ineffective Th1 differentiation and polarization, which is essential for the control of M. avium infection. In addition, absence of CD38 seems to compromise the maintenance of the granulomatous barrier, leading to dissemination and unrestrained growth of mycobacteria. 
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 +CD38 Controls the Innate Immune Response against [[https://iai.asm.org/content/81/11/4091|Listeria monocytogenes]] 
 +Using a murine Listeria monocytogenes infection model, we found that CD38 knockout (KO) mice were highly susceptible to infection. Enhanced susceptibility was already evident within 3 days of infection, suggesting a function of CD38 in the innate immune response. 
 +CD38 was expressed on neutrophils and inflammatory monocytes, and especially inflammatory monocytes further upregulated CD38 during infection. Absence of CD38 caused alterations of the migration pattern of both cell types to sites of infection. 
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 +In vitro, macrophages of CD38 KO mice were less efficient in uptake of listeria but still able to kill the bacteria. Dendritic cells also displayed enhanced CD38 expression following infection. However, absence of CD38 did not impair the capacity of mice to prime CD8+ T cells against L. monocytogenes, and CD38 KO mice could efficiently control secondary listeria infection. In conclusion, our results demonstrate an essential role for CD38 in the innate immune response against L. monocytogenes. 
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 +===== At this time there are no AIDS patients on the Marshall Protocol =====
  
  
home/diseases/hiv_and_aids.txt · Last modified: 09.14.2022 by 127.0.0.1
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