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Report From San Francisco I: The “Father of Autoimmunity” Speaks

March 31, 2014

When the "Father of Autoimmunity' went to medical school 'autoimmunity' was not believed to exist

When the “Father of Autoimmunity’ went to medical school ‘autoimmunity’ was not believed to exist

Dr. Noel Rose M.D., PhD is  the Director of the Center for Autoimmune Disorders at Johns Hopkins University. Dr. Rose has been studying autoimmunity for over sixty years  but he was a pretty darn spry 80-something at the conference.

When I got close enough to  ask him a  quick question I would have sworn he was a well-preserved sixty something. The bow tie,though, still apparently in  fashion in some medical circles, gave it away as did his statement that the medical schools of his day scoffed, yes, scoffed at the idea that the body could attack itself.

In fact, in 1956 Dr. Rose was the first researcher to introduce autoimmunity as a cause of disease. In an interview he stated

“They were skeptical. People weren’t really prepared to believe it because it seemed so bizarre that you would develop an immune response to your own body. We had all been taught in medical school that the immune response is only directed to what’s foreign. But now we know that isn’t true.”

He’s one of the few people who could can say they wrote the book on it because he did. He wrote the first book on autoimmunity and it’s still being revised today. (Get the latest 1300 page edition for a cool $215)

Dr. Rose probably didn’t appear to know a lot about Chronic Fatigue Syndrome, but he does know  a lot about autoimmunity and with the Rituximab trials putting that subject on everyone’s mind it was good to get a primer on it.

Dr. Rose started off explaining the basics of the autoimmune response by stating that it’s a completely  natural response. We’re all doing autoimmune responses all  the time.  The reason for that is that ‘we all’; that is all the organisms on earth,  share proteins and enzymes and that means that the immune system is going to, in its fervor to rid the body of a pathogen, will inevitably accidentally attack the body instead at times. That means we  come loaded from the get-go with auto -antibodies and  self reactive T and B-cells and also that  we have a built-in way of suppressing those cells.

It’s when that suppression system goes down that you have trouble.

Males and females generally have equal rates of autoimmunity until puberty when the hormones kick in. Rates begin to even out  more in seniors

Males and females generally have equal rates of autoimmunity until puberty when the hormones kick in. Rates begin to even out more in seniors

An autoimmune response can affect essentially any organ disease in the body, and while  autoimmune disorders can show up very differently, they also share many features. They’re common – they’ve been diagnosed in about 20 million people in the U.S., but probably closer to 50 million Americans have one. They’re ‘chronic’  (usually life-long). They mainly affect women and they’re heavily hereditary.

There are no known cures, they’re expensive – costing the U.S. about a hundred billion (gulp) dollars yearly, and, in contrast to cancer and heart disease, they are on the rise.  About 80 autoimmune diseases have been identified and more are coming.

To the question why there are so many autoimmune  diseases, he stated

 “We think it’s the fact that the immune system is always looking for new pathogenic organisms and being very broad in its abilities to recognize organisms that it also responds to things within our own bodies that are of the same or a very similar substance.”

 

The Sex Bias

Hormones clearly play a major factor in the female predilection for autoimmune disorders.  Rates of autoimmune disorders in children  prior to puberty are equal  in males and females and pregnancy can have a huge effect on symptoms, with some women feeling much better.

They’re believed to  mostly result when  a genetic weakness plus an endocrine effect (female bias) bumps up against an environmental trigger such as an infection. Bad genes account for thirty percent of  the risk which means that 70% of it is probably some chance environmental factor you would have surely avoided if only you’d known.

Known environmental triggers include viruses (in particular EBV), bacteria (streptoccocus), drugs, foods (excess salt), pollutants such as mercury, hormones, stress (important but hard to quantitate). Because the exposure usually comes months or even years before you come down with an autoimmune disorder finding, the triggering factor is  often very  difficult.

gene

Genes account for 30% of the risk for getting an autoimmune disorder. Environmental triggers (infection, toxin, stress, drug) are far more important.

Celiac disease is one of the few autoimmune disorders in which the triggering factor is clear: gluten. Gluten-free diets may be important for more than Celiac patients, however. Dr. Rose believes they  can help people with other kinds of autoimmune disorders.

“Interestingly,” he added, “the gluten free diet may also be helpful for people who don’t have celiac disease but who have other forms of autoimmune disease. It’s just speculative, but as gluten free diets are more available, other people are trying them and often feel better.”

If you have a family member with an autoimmune disorder your risk of developing one jumps over 10-fold (from  .4% to 7%). If your twin has an autoimmune disorder you’ve got a 30% chance that you will come down with one  as well.

Once autoimmunity gets going it usually causes more damage and inflammation and generates more autoimmunity. One of the common signatures is  multiple autoantibodies to multiple antigens.

Treatment

Like ME/CFS and many other chronic illnesses, treatment is focused on symptom alleviation not curing the disorder. Progress is being made, however.

 “We still don’t have a cure, but new treatments have been introduced in the past 15, 20 years for autoimmune diseases like lupus and MS that are remarkable and very much improved. As we understand more about the autoimmune response we find more ways of developing drugs that will intervene, that will benefit the patient by at least alleviating the symptoms even if they won’t cure the disease.”

Autoimmune or Autoinflammatory?

Some disorders that have a strong inflammatory component and look like autoimmune disorders  are not auto-immune disorders; they’re auto-inflammatory disorders.  People with the autoinflammatory disorders carry  loads of auto-antibodies, but lack the self-reactive T and B cells found in true autoimmune disorders.  With regards to treatment  it’s often  a distinction without a difference because both involve the  innate immune system and they’re often  treated the same way.

innate immune diagram

Problems with the innate immune system (NK cell, neutrophils, complement, histamine, etc. ) are behind autoinflammatory disorders

The term  autoinflammatory only showed up in the scientific literature for the first time in 1990′s. Autoinflammatory disorders involve dysregulation of the innate immune system (NK cells, dendritic cells, macrophages,etc.) that result in high rates of inflammation.

Autoinflammatory disorders originally included ‘recurrent fever syndromes’, then branched out to include some genetic disorders, hard to understand disorders like Crohn’s disease, and now may include such common disorders as type II diabetes, gout and atherosclerosis. The  decreased adaptive immune response and increased innate immune response found in autoinflammatory disorders suggest aging could be included in this category. (In the Conference we’ll see some preliminary evidence of increased aging in ME/CFS)

We don’t know if some  individuals with ME/CFS have an autoimmune or an autoinflammatory disorder. Rose didn’t appear to know much about ME/CFS but after his  talk I asked Rose what I thought was THE question; the question that was not given to him  during the Q&A session even though I wrote it out twice,  the second time at least semi-legibly, and  that was:

“What does a positive response to Rituximab in a gender  specific disorder tell you about autoimmunity or  an auto-inflammatory response?” The MAN said it meant it could be either.

 ME/CFS Autoimmune Studies Underway

 ”We hope this study will identify a pathogen as a likely causative agent of the disease in order to focus future study. Dr. Elledge

dorsal root ganglia

One CFIDS Association of America study will target autoantibodies to the dorsal root ganglia that the Light’s believe play a role in ME/CFS

Besides the two Rituximab trials two studies, both using the CFIDS Association of America’s Biobank, will shed light on the role autoimmunity plays in  ME/CFS. One promising study lead by Dr. Elledge of Harvard University will determine what the autoantibodies present in ME/CFS patients blood are targeting and what viruses the antibodies present are associated with.

“…autoantibodies to brain and dorsal root ganglia have been demonstrated in chronic post-Lyme disease syndrome, an entity essentially identical with chronic fatigue syndrome/fibromyalgia” Dr. Cooperstock

Another lead by Dr. Cooperstock will look for autoantibodies to nervous system targets including the dorsal root ganglia that feature in some theories of ME/CFS.

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9 Comments

  • Issie

    April 1, 2014 at 2:58 am - Reply

    I agree, most of our illnesses seem to be explained by autoimmune system dysfuncton and inflammation.

    Enjoyed your blog on this, Cort.

    Issie

  • Angela

    April 1, 2014 at 3:55 am - Reply

    Chronic post Lyme disease syndrome is nonsense. It’s chronic Lyme disease and all the damage it causes. They need to read “Why Can’t I Get Better?” by ILADS Dr Richard Horowitz.

  • geoffrey keith brown

    April 1, 2014 at 5:27 am - Reply

    I wish somebody with the necessary brains would take this up and run with it

    • Teresa

      April 6, 2014 at 1:03 am - Reply

      i know lol

  • Claire

    April 1, 2014 at 3:12 pm - Reply

    Fascinating stuff.
    I recently read, and would highly recommend to everyone, the 2012 New York Times Best Seller, Brain On Fire, by Susannah Cahalan. It is an autobiography about her recent brush with death after she developed an auto-immune disease in which she developed auto-antibodies to a protein, NMDA receptor, in her brain. Having this auto-antibody caused an encephalitis that mimicked schizophrenia. It was only discovered in 2007. Prior to that, people with this would either end up in psychiatric hospitals or would die. Even in 2012 (and possibly now) many doctors would miss this diagnosis.
    Could ME/CFS be due to an auto-antibody to a protein in the central nervous system , I wonder?

  • Lisa Petrison

    April 1, 2014 at 9:31 pm - Reply

    Thanks for reporting on this, Cort. What seems critical here is the fact that autoimmune diseases have become so much more prevalent in recent years than they were in the past. Certainly there could be reasons for this other than environmental toxicity, but if we’re going to look at what has changed over the past 50 years, the toxins would be in first place by a long distance. If I ever had a chance to meet Dr. Rose, I thus would ask him whether it might be possible that the body is not reacting to “itself” but rather to contaminants — meaning the toxins that are stored inside it. If that did turn out to be the case, it would explain why none of the medical treatments for “autoimmune” diseases of any sort have been successful and also might possibly send us off in a whole new direction with regard to approaching the problem.

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