 |
| Author | Post |
|---|
Joyful
Board Staff
| Joined: | Sat Jun 9th, 2007 |
| Location: | Restville, Again |
| Posts: | 1708 |
| Status: |
Offline
|
|
Posted: Sun Feb 22nd, 2009 00:01 |
|
Here we go again, trying to use correlation to jump straight to causation.
Ok, I know you call it ...Evidence Based Medicine... (neanderthal in a white coat  ?)
I found the video overall to be very sad. Lots of people telling their stories of how their disease has impacted their life, then researchers explaining how the disease processes are poorly understood. Then doctors and others explaining how there are no effective treatments, only palliative care.
I was a little concerned when one researcher stated that all autoimmune disease is lympatic in nature. (At least that is what I remember hearing him say.)
I believe you, Dr. Marshall, have some good news for the Lymphatic Research Foundation... 
...the cause is the same as for Th1 disease ... and there is a treatment! 
Edit: forgot the link... http://www.lymphaticresearch.org
Last edited on Sun Feb 22nd, 2009 00:29 by Joyful
____________________
Lyme?1980 Lyme/Babs/Bart?05 CFS?06 | Start 125D(50) 25D(32) Jun07 | Ph1Jul07 ModPh2Sep07 Ph2Feb08 Ph3Aug08 | Latest 25D(9) Apr09 | ABC of MP
|
Markt9452
Member in Phase 3
|
Posted: Tue Mar 3rd, 2009 02:39 |
|
New origin found for a critical immune response DURHAM, N.C. – An immune system response that is critical to the first stages of fighting off viruses and harmful bacteria comes from an entirely different direction than most scientists had thought, according to a finding by researchers at the Duke University Medical Center.
"This finding will have important implications in vaccine science and autoimmune disease therapy development," said Michael Gunn, M.D., an immunologist and cardiologist at Duke and senior author of the study published in Nature Immunology.
Type 1 helper (TH1) T cell immune responses are critical for the control of viruses and certain bacteria. Immunologists have generally believed that TH1 responses are induced by rare immune cells, called dendritic cells. When activated by infection or vaccination, the dendritic cells were thought to move from peripheral tissues into lymph nodes to stimulate T cell responses.
The Duke researchers found, however, that the dendritic cells that stimulate TH1 responses didn't come from peripheral tissues, but rather arose from monocytes, a common cell type in the blood, that moved directly into lymph nodes after infection.
"The result speaks to the most basic principles of immune response to pathogens," Gunn said. "It may also explain the poor results we have seen in attempts to develop effective dendritic-cell vaccines."
Gunn previously had identified a particular protein, known as a chemokine, that stimulates the migration of activated dendritic cells from peripheral tissues to lymph nodes. The Duke researchers generated a TH1 response in laboratory mice that lacked this chemokine with influenza viruses.
"We really thought the mice would not be able to generate much of an immune response at all," Gunn said, because they wouldn't be able to mobilize dendritic cells. "The mice, however, had increased TH1 responses. We knew we had to find what was really causing the response."
One scientist who knew about these findings told Gunn the Duke group would "never figure this out" because their findings were so unconventional.
To solve the mystery, the Duke team studied several different types of mice, which were missing other chemokines or chemokine receptors. They found that mice without the Ccr2 chemokine receptor that controls the migration of inflammatory monocytes had much lower accumulation of monocyte-derived dendritic cells and TH1 responses.
The scientists concluded that there is a blood-derived lymph node dendritic cell type that has a key role in developing acute T-cell responses. "For so long, dendritic cells from tissues were the obvious answer," Gunn said. "We found out that that's not always the case."
The team now plans to look at the blood-derived dendritic cells under different conditions to see if they may have other activities. "We observed the activity of these cells after TH1-inducing stimuli, like influenza," Gunn said. "Next we'd like to study other types of immune stimuli to see how the cells respond."
Understanding how dendritic cells stimulate different types of immune response would open the door to enhancing or inhibiting these responses, a major goal of immunologists trying to prevent infections or control autoimmune disease, Gunn said.
### The work was supported by grants from the National Institutes of Health.
____________________
Th1 Lyme Symptoms 125D20 D2510 Ph1Feb08 Ph2Apr08 Ph3Oct08 daily med.exp covered up NoIRs| MyStory|
|
Joyful
Board Staff
| Joined: | Sat Jun 9th, 2007 |
| Location: | Restville, Again |
| Posts: | 1708 |
| Status: |
Offline
|
|
Posted: Tue Mar 3rd, 2009 08:01 |
|
Good find Mark!
Thanks.
____________________
Lyme?1980 Lyme/Babs/Bart?05 CFS?06 | Start 125D(50) 25D(32) Jun07 | Ph1Jul07 ModPh2Sep07 Ph2Feb08 Ph3Aug08 | Latest 25D(9) Apr09 | ABC of MP
|
kenc
Member in Phase 3
|
Posted: Tue Mar 3rd, 2009 08:40 |
|
The immune system appears to be more complex and convoluted as more discoveries are made about it.
When I presented the MP to my gastroenterologist he responded by saying, "I'm skeptical because it can't be that simple. The immune system is too complex." He had done research on Crohn's disease in the past and was currently doing research on Hepatitis B. He always had been leaning towards a microbial cause for Crohn's and other so called autoimmune diseases. So he was supportive of the general direction of the MP. He just found it hard to believe that the MP would work.
For the MP to succeed in all cases, wouldn't it ultimately have to enable the immune system to target all pathogens? Are there any receptors other than the vitamin D receptors that are essential to the immune system function? If so, could these also be impeded by bacterial antagonists?Last edited on Tue Mar 3rd, 2009 08:45 by kenc
____________________
Crohn's Disease 1984, 24May05 1,25D=33 25D=8.4, 6Sep05 1,25D=29 25D=12, 11Jun07 25D=<10.4 1,25D=10, 15Sep07 1,25D=14.2 25D=16, 12Jul05 Phase1 + pred, 12Jul06 Phase2 + pred/dexa, 14Aug07 Phase2, prednisone, dexamethasone, testosterone, aspirin, levothyr
|
jlunn247
Member in Phase 3
| Joined: | Fri Jul 27th, 2007 |
| Location: | Michigan USA |
| Posts: | 109 |
| Status: |
Offline
|
|
Posted: Tue Mar 3rd, 2009 08:52 |
|
maybe serotonin?
____________________
Sarc/lungs/joint pain TMJnerve pain 125D56 25D16 Ph1Mar07 ModPh2Jun07 Ph2Nov07 PHase3Feb08 albuterol
dark sunglasses hands & face exposed. Medium herx
mostly.june09
|
Frans
Member in Phase 2
|
Posted: Tue Mar 3rd, 2009 09:35 |
|
Well,
At least the other type I nuclear receptors.
I am not sure if capnine has an affinity for those, but 1,25D and 25D dó have an affinity for those.
So if 1,25D goes too high, those other receptors , like PXR will be blocked. I remember Trevor posting that some of these receptors also express AMPs.
At least, that is what Trevor posted a day or 2 ago.
Check his last posts. Above his photograph, click on his name, hoose, 'View profile' and then choose the tab: 'Posts'.
This gives you a list of all Trevor's posts.
Activating VDR will lower 1,25D (and 25D) wchich willl lead to those other receptors to start working ok again.
Yes, it is that simple
Hope this helps, Frans
____________________
Burn-out/nervous breakdown Jan01 125D 48 25D8.48 Ph1Nov06 ModPh2Jan07 Ph2Apr08 Cipramil Seroquel NoIRs lite exp r/t work cover up 25D3.9(Oct07)
|
Dr Trevor Marshall
Research Team
|
Posted: Tue Mar 3rd, 2009 16:30 |
|
I'm skeptical because it can't be that simple. The immune system is too complex
The concept that a metagenomic microbiota is interfering with gene transcription and DNA repair in Homo sapiens, and probably all other life (similar pathogens have been observed in worms from coral reefs), is relatively simple.
The thousands of genes interacting, and the complexity of the interactions, are beyond comprehension. That is the hard part.
Our big breakthrough was to understand how the microbiota was disabling the innate immune system, and figure out how to correct that. Additionally, we were able to realize that all chronic diseases could all arise from different genetic interactions resulting from a ubiquitous microbiota.
Last edited on Tue Mar 3rd, 2009 18:32 by Dr Trevor Marshall
|
kenc
Member in Phase 3
|
Posted: Tue Mar 3rd, 2009 22:54 |
|
| By following the protocol, are we reactivating all parts of the innate immune system or could there still be other parts being disabled or down regulated by bacterial ligands?
____________________
Crohn's Disease 1984, 24May05 1,25D=33 25D=8.4, 6Sep05 1,25D=29 25D=12, 11Jun07 25D=<10.4 1,25D=10, 15Sep07 1,25D=14.2 25D=16, 12Jul05 Phase1 + pred, 12Jul06 Phase2 + pred/dexa, 14Aug07 Phase2, prednisone, dexamethasone, testosterone, aspirin, levothyr
|
Dr Trevor Marshall
Research Team
|
Posted: Wed Mar 4th, 2009 00:19 |
|
Well, as the bacteria are killed, there become no bacteria left to down-regulate anything
|
Ruth Goold
Health Professional
|
Posted: Wed Mar 4th, 2009 19:42 |
|
Interesting article published in Nature today by Torchinsky et al. showing that when neutrophils infected with bacteria undergo apoptosis, the TH17 cell pathway is induced (leading to inflammation and autoimmune conditions). On the other hand, when uninfected neutrophils undergo apoptosis, the anti-inflammatory Treg pathway is triggered. I’ll add the PubMed ID when it is available.
An excerpt:
“Cell death results in immunological consequences determined by molecular components intrinsic to dying cells and specific to the nature of the trigger for cell death26. Our findings illustrate how the immunosuppressive nature of apoptotic cell clearance27 can coexist with the necessarily inflammatory nature of infection, and assign an important role to phagocytosis of apoptotic cells in contributing signals which, in combination with TLR engagement, induce tailored immunity to bacterial infection through development of TH17 cells. Apoptosis in the absence of TLR engagement leads to tolerance through development of Treg cells.
Our results also explain why some but not all microbial pathogens induce TH17 cells, and indicate the importance of examining apoptosis induction by these pathogens.”
Ruth
____________________
03/02/07 Ph 1 MP; 2001: Pulmonary sarc; 01/04/07: 125 D=110pmol/L(45.8 pg/ml)| 25D=20.8 ng/ml: 04/07 19.2: 07/07 11?: 09/07 16.5: 11/07 <10.0: 01/08 <10.0: 05/08 10 ng/ml. Ca. Elocom (ears). diphenhydramine 25 mg. Adidas EE glasses outside. NoIRs
|
jlunn247
Member in Phase 3
| Joined: | Fri Jul 27th, 2007 |
| Location: | Michigan USA |
| Posts: | 109 |
| Status: |
Offline
|
|
Posted: Thu Mar 5th, 2009 04:30 |
|
I studied the enbrel Medicine for psoriasis during a double blind phase four trial
And found that it was an immune suppressor that down regulated the inflammatory cells and dis regulated the accelerated skin cell growth.this was in 1999 or maybe 2001
The risks of treatment outweighed the problems associated with the disease.
Last edited on Thu Mar 5th, 2009 04:33 by jlunn247
____________________
Sarc/lungs/joint pain TMJnerve pain 125D56 25D16 Ph1Mar07 ModPh2Jun07 Ph2Nov07 PHase3Feb08 albuterol
dark sunglasses hands & face exposed. Medium herx
mostly.june09
|
jcwat101
Research Professional
| Joined: | Tue Jul 20th, 2004 |
| Location: | Pasadena, USA |
| Posts: | 1430 |
| Status: |
Offline
|
|
Posted: Thu Mar 5th, 2009 05:30 |
|
Ruth,
I think that paper is very important, since Th17 is seen as particularly relevant in autoimmune disease now -- sounds to me like this is likely to be great support for the idea of infected white blood cells -- like we talk about.
And it helps that it is coming out in Nature.
Joyce Waterhouse
____________________
20 yrs with CFS/FM/Lyme/IBS, food sensitivities; 1,25D/25D 8/04:64/11 http://SynergyHN.com
|
Lee
Member in Phase 3
|
Posted: Fri Mar 6th, 2009 15:17 |
|
Has this subject been discussed? I find it interesting! I apologize if it has been yakked about already ! Lee
In our patients sarcoidosis developed after 2 years of continuous treatment with infliximab and adalimumab. Both patients presented with low-grade fever, chest pain, and dyspnea. The diagnosis of sarcoidosis was established by the typical well-formed noncaseating granulomas on transbronchial biopsy, after excluding all other granulomatous conditions. Following withdrawal of anti-TNFα agents and a brief course of steroids, the clinical picture resolved. Thirteen additional cases of sarcoidosis that developed after anti-TNFα treatment have been reported, and in 9 of these the causative agent was etanercept.
Conclusions
The development of sarcoidosis during treatment with TNFα antagonists represents a rare and paradoxical adverse event. The occurrence of sarcoidosis with all 3 available agents suggests a new “class effect” probably linked to a cytokine disequilibrium in patients receiving anti-TNFα treatment.
Keywords: sarcoidosis, infliximab, adalimumab, TNF-α
Article Outline
____________________
2003 SARC w/COPD Hyper-Flex Fibro.
D ratio-2.13 Ph1-2/05 Benicar| 4/05 PH2| 06 Ph3| 2008 D25-9.7 silymarin/sunlight w/noirs
|
Current time is 20:44 | |
|
|
|
|
