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Autoimmune Diseases: The Invasion of the Body by the Body          

            All autoimmune disease is a result of the body's immune system "attacking" itself.  For whatever reason, your body gets a signal to mount an attack on "self" - basically on certain types of tissues or cell types in the body.  This is not a natural event, thank goodness; when the body attacks itself, something quite bizarre has to be going on inside.  The Big Question has always been, "what makes this happen?" The even bigger question has always been, "What can you do about it?" We are much closer to the answer.

            In rheumatoid arthritis, for example, the primary targets are the joints.  In scleroderma, the attack is mounted on skin and connective tissue.  Generally speaking, the primary pathology of autoimmune disease is inflammation, as different cells and tissues are assaulted and become inflamed.  In both of the instances mentioned above there are many other far-reaching effects due to inflammatory reactions elsewhere in the body.  There is no mystery in the primary issue here - inflammation - just a mystery as to how and why it happens.

            Saying, "the immune system," is really an attempt to simplify an immensely complicated equation.  The immune system has many ways to mount a response.  The three basic ways (there are others) are: 1) by producing antibodies, 2) by using T-cells and 3) by way of literally scores (probably thousands) of inflammatory "mediators".  Although all of these mechanisms are involved in autoimmune disease to some extent, it is the T-cell response that interests me, and may be the most critically important.  Since LDA immunotherapy is T-cell mediated (works by stimulating certain T-cells), it is only logical that if you could tailor LDA to have a beneficial effect on the T-cells involved in autoimmune inflammation - say in rheumatoid arthritis - you'd really have something.  Well, Dr. Len McEwen - the discoverer and developer of EPD - found a way.  It has to do with a principal called molecular mimicry.

Molecular mimicry      

            Molecular mimicry is generally interpreted as the sharing of molecular structures (or their protein products) by portions of dissimilar genetic material (i.e. "resemblance" or cross-reactivity, most often between different organisms).  This produces an "error in identification" by the host.  The mimicking material is usually foreign ("non-self" e.g. bacteria) but the material contains at least one protein component similar enough to certain host cells that the host then gets confused. A T-cell identifies the protein, but a segment of the protein is so similar to "self" - in fact, exactly similar - that the T-cells instead of attacking or dealing with the bacteria, mount an attack on "self."  In other words, a bacteria can trick the body into attacking its own normal cells that have a few very precise characteristics of a bacterial protein.  When you think a lot about this, as I have, the prospect is extremely frightening, especially if there are significant numbers of those hanging about.

Major histocompatibility (MHC) and the relationship to human leukocyte antigen (HLA)

Discussion of molecular mimicry requires a short talk about HLA receptors, since that's where mimicry takes place.  So please bear with me.  If you have autoimmune disease, and you understand this, you will have an amazing revelation as to why mimicry is so important to your illness.

Major histocompatibility (MHC) molecules (generally referred to as receptors) are of two major types - Class I and Class II.  A third type (Class III, not discussed here) is a subset of serum proteins involved in the complement system.

Class I MHC receptors are found on the surfaces of all somatic (body) cells and are unique to every individual.  These molecules, or receptors, appear on the cell membrane.  No two individuals have exactly the same combinations of MHC Class I receptors.  It follows that these receptors govern "non-self" recognition and are responsible for phenomena such as graft rejection.

Class II MHC receptors are found on the surfaces of macrophages and lymphocytes, and are likewise expressed on their cell membranes.  They provide the self-recognition necessary to interact with one another and with other immunocompetent cells.  Many people have comparable Class II receptors.

 Human leukocyte antigen (HLA) receptors are simply a type of MHC receptor molecule.  HLA receptors may be either Class I or Class II MHC receptors.  Many scores - if not hundreds - of HLA receptors have been identified, and there are most likely very large numbers present on most all human cells.

HLA-B27, for example, is a class I MHC receptor that may be found on cells in the body (somatic cells).  However, an individual must possess a specific genetic trait (inherited on the sixth chromosome) in order to produce this type of receptor.  About 7% of the population in the USA is HLA-B27 positive, although certain specific or isolated populations may average considerably higher.

            One place where mimicry frequently occurs has been identified specifically as this HLA-B27 receptor.  When molecular mimicry occurs, the body then targets cells elsewhere in the body (in tissues and organs) possessing these same receptors.  These cells may be those of synovial tissue, mucous membranes, connective tissue, skin, the central nervous system or other body cells, tissues and organs, and the immune response is generally adverse, affecting that tissue or organ.

            The HLA-B27 genotype has been the most studied HLA receptor site, and is of particular importance to me and the concepts presented here.  There is now little question that it represents one of the "classical" and certainly the most common site where molecular mimicry takes place.  Importantly, HLA-B27 has been associated with various spondyloarthropathies, and with a type of arthritis called "reactive" arthritis (severe, usually fluctuating joint pain and inflammation without antibodies for rheumatoid arthritis or autoimmune disease, which constitutes most types of autoimmune arthritis).

           The final result is that the body mistakenly mounts and propagates an assault against "self" just because some incorrect information has been received from an outside "non-self" source.  The effects and ramification of mimicry on human tissue are critically important, and the proposed mechanism and the results of this "sharing" which occurs with molecular mimicry will be discussed in the material that follows.

The relationship of HLA to ankylosing spondylitis, rheumatoid arthritis and other illnesses

            Evidence of the first links of HLA receptors to ankylosing spondylitis occurred in 1973, when it was found that there was a higher occurrence of ankylosing spondylitis in patients with certain HLA subtypes.  However, Ebringer's studies (see references at the end of this section) were paramount in the identification of HLA-B27 and the concept of mimicry caused by the Klebsiella bacteria at that site.  They were also crucial in the development of the concept that the arthritis associated with ankylosing spondylitis was actually a reactive arthritis secondary to mimicry.  Ebringer also demonstrated that HLA-B27 is expressed on the lymphocytes and synovial cells (cells in the joint spaces) of virtually 100% of patients with ankylosing spondylitis, as compared to 7% in most populations.

The presence of specific anti-Klebsiella antibodies in patients with ankylosing spondylitis during the acute phase of the disease clearly indicates these patients have been exposed to these specific bacteria.  Ebringer proposed that the subsequent immune response then causes a "reactive arthritis", especially in patients positive for HLA-B27. The concept of reactive arthritis is important.

            Many other works have appeared that confirm the association of the genetic HLA-B27 trait and the concept that Klebsiella functions via molecular mimicry in the etiology of ankylosing spondylitis and other similar conditions.  The bottom line is that Klebsiella is an important - if not major - cause of ankylosing spondylitis. Of course, not all people who are HLA-B27 positive have this disorder, but certainly none without this receptor have it.

Rheumatoid arthritis

Strasny made an association with the B-cell HLA receptor DRW4 and rheumatoid arthritis as early as 1973.  While Ebringer and others were investigating ankylosing spondylitis and its association with Klebsiella, HLA-B27 and molecular mimicry, these and other authors were studying the association of rheumatoid arthritis, Proteus, HLA-DR4 (and HLA-DR1) and the identical principal of molecular mimicry. The incidence of the genetic disposition for HLA-DR4 in most of these studies of patients with rheumatoid arthritis has varied between 50-75%.  Up to 93% of patients with rheumatoid arthritis are apt to carry both HLA-DR1 and HLA-DR4.

            Similarities between the work of Ebringer and others who associated HLA-B27 and Klebsiella to that of many other authors who associated Proteus and HLA-DR4 made the case of molecular mimicry in both diseases quite beyond question.

Reactive arthritis and inflammation

Although the direct association of at these two organisms to ankylosing spondylitis and rheumatoid arthritis via molecular mimicry was important, the relationship of yet other organisms to yet other disorders has been taken this a crucial step further.  Indeed, much of the initial focus of the studies cited above turned eventually to the "reactive" components of autoimmune and other disorders as critically important doctrine.

The term "reactive arthritis" encompasses most all forms of arthritis where blood tests are negative (including ankylosing spondylitis).  Reactive arthritis is an important concept to me, as the published literature has caused me and others to feel that the majority of the different types of reactive disorders may well be autoimmune events.

Since 60-80% of patients with reactive arthritis are positive for HLA-B27, one would have to consider that these inflammatory disorders might also likely be associated with molecular mimicry.  Many authors have since drawn this conclusionMuch has appeared in the literature demonstrating that reactive arthritis (and other disorders, some discussed below) may be induced by a variety of organisms, and is by no means confined to Klebsiella and Proteus organisms.

Various types and species of intestinal organisms have now been clearly shown to cause rheumatoid or non-rheumatoid (reactive) arthritis in patients, in addition to Klebsiella and Proteus.  This list includes, but is certainly not limited to: Strongyloides stercoralis, Taenia saginata, Endolimax nana, Dracunculus medinensis, Giardia lamblia, Yersinia enterocolitica, Shigella, Salmonella, Campylobacter, Clamydia, Hemophilus influenza, E. coli, Bacteroides  and numerous others.

Gastrointestinal disorders can themselves be due to bacteria via mimicry, even though the intestine may be the natural habitat of the bacteria involved.  This includes gastritis, irritable bowel syndrome, ulcerative colitis and others. Foods may also cause intestinal disorders by way of mimicry Other inflammatory disorders, many of them autoimmune, have been studied in relation to molecular mimicry caused by various organisms.

Other examples of illnesses that have been attributed to molecular mimicry and organisms are primary biliary cirrhosis by urinary tract bacteria, hepatic stenosis or inflammation by Bacteroides, experimental colitis by anaerobic bacteria, juvenile dermatomyositis and necrotizing arteritis by streptococcus, and arthritis by H. influenza meningitis. This is only a small sampling of the growing link between bacteria, inflammation, autoimmune disease and molecular mimicry.

The anaerobe, Bacteroides has been of particular interest to me and others.  Predominantly anaerobic bacteria proliferate in blind loop animal (and human) models, and the resultant vitamin B-12 deficiency, iron loss and protein-losing enteropathy has been reversed by metronidazole and tetracycline, both of which target Bacteroides spp.

Bacteroides has been shown to be a major cause of reactive arthritis, liver disease and dermatitis, and it has also been demonstrated that patients with these complications resulting from jejuno-ileal bypass for obesity responded to metronidazole, a drug rather specific for Bacteroides.

One would postulate that if bacteria associated with molecular mimicry could cause disease, the use of other appropriate antibiotics might provide temporary (or even long-term) relief for patients suffering with a disease caused by mimicry.  This has been demonstrated by several authors, and is probably the reason Dr Thomas Brown's low-dose tetracycline protocol works for many patients with rheumatoid arthritis.

Molecular mimicry: the mechanism and its ramifications

            Perhaps the most complete and comprehensive scenario to help one to understand the concepts of molecular mimicry was developed by Oldstone, Schwimmbeck, Yu and colleagues, spanning a series of 14 published papers, beginning in 1972 and culminating in 1989.  These authors have provided a likely model for the primary mechanism for molecular mimicry.

Srinivasappa and colleagues tested over 600 of these monoclonal antibodies, all directed against specific viral polypeptides.  They then charted the cross-reactivity of these same monoclonal antibodies with host proteins expressed by a large variety of normal tissues.  Through their testing, corroborated by Oldstone, the monoclonal antibodies selected reacted with 14 different viruses.  These included both common RNA and DNA viruses, such as herpes, human retroviruses, vaccinia and others.  Most importantly, over 4% of the monoclonals reacting with the viruses cross-reacted with host cell protein expressed on uninfected tissues, and some with more than one host organ.

            This observation showed that molecular mimicry (cross-reactivity) is indeed common and not necessarily restricted to any particular class, virus or group.  It demonstrated that many viruses share specific antigenic groups with normal host cells, tissue and organ proteins.

Oldstone then proved experimentally that molecular mimicry could cause autoimmune disease, as had been advocated and proven by Ebringer and others, primarily via mimicry at HLA-B27.  To do this, Oldstone's group chose myelin basic protein or MBP for study, a major component of nerve sheath, because its entire amino acid sequence is known.  Also critical, the encephalitogenic site where myelin basic protein is attacked to produce encephalitis is a recognized sequence of 8-10 amino acids, and it has been mapped on several animal species.

Using computer-assisted analysis, they found that several viral proteins showed similar amino acid sequences closely matching just the encephalitogenic site of MBP in the rabbit.  The closest was hepatitis B virus polymerase (or HBVP). Of the 8-10 amino acid sequence at the encephalitogenic site of MBP, six sequential amino acids in HBVP matched.

            When rabbits were inoculated with either the 8 or the 10 amino acid peptide fractions, both the humoral and the cellular products produced in the rabbits' tissues and serum reacted against whole myelin basic protein.  The peptide also caused perivascular infiltrates localized to the rabbits' CNS, similar to that produced by inoculation of whole MBP or just the MBP fragment containing only the encephalitogenic site.  The matching site was the six amino acid sequence Tyrosine-Glycine-Serine-Leucine-Proline-Glycine.  The rabbits did not contract hepatitis, but contracted encephalitis due to mimicry.

            This conclusively showed that molecular mimicry, caused by injection of a non-homologous (not from the same species) amino acid peptide containing a known sequence of only six amino acids matching a site on host protein could cause both autoimmune humoral (antibody) and cellular responses, and cause autoimmune disease itself.

Perhaps the most convincing paper to describe the mechanism of a "mimic" involved with molecular mimicry was published by Husby, Tsuchiya, Schwimmbeck and colleagues, (Oldstone included) in 1987.  This time they found a sequence of six amino acids, QTDRED, in Klebsiella pneumoniae nitrogenase that was exactly the same as that of the HLA-B27 antigenic epitope (the actual HLA-B27 receptor protein).

When Husby and associates used rat antiserum reactive to HLA-B27 and antiserum to Klebsiella pneumoniae nitrogenase to stain the synovial tissue of patients with ankylosing spondylitis or reactive arthritis, they repeatedly demonstrated cross-reactivity: both stained the synovial tissue.  The part of the HLA-B27 antigen encompassing the QTDRED sequence was strongly expressed on the synovial joint lining cells of 11 out of 12 patients with ankylosing spondylitis, which confirmed the impression that direct molecular mimicry was taking place at the actual tissue level.  The possibility of a six amino acid sequence being the same in two dissimilar protein species is 1 in 620, so there is little doubt as to the validity of this observation.

Several other investigators have demonstrated amino acid homology between organisms and host tissue (Table 6).  There is still debate as to the precise mechanism of mimicry, such as whether a "superantigen" is involved at HLA-B27 and elsewhere, or whether mimicry is a reaction to an antibody.  However, the concept as a whole remains concrete.

A rapidly growing number of autoimmune diseases are associated with HLA-phenotypes.  Certainly HLA-B27 has been associated with ankylosing spondylitis, reactive arthritis, autoimmune thyroiditis, "reactive" hepatitis, inflammatory diabetes and Reiter's syndrome.  HLA-DR4 has been associated with rheumatoid arthritis.  We now know that Sjogren's syndrome occurs more commonly in patients who are HLA-B8, HLA-DR3 or HLA-DRW-52 positive; scleroderma occurs more commonly in those who are HLA-DQ+ positive.  Behcet's disease has shown to be associated with HLA-B51.

The primary purpose of the preceding discussion is to demonstrate that a phenomenon exists allowing host cells to inappropriately misidentify foreign protein and, as a result, mount an attack upon the body itself instead of the foreign protein.

The T-cell, mimicry and autoimmunity

In 1993, Hermann and Yu tested CD8 T-lymphocyte clones derived from the synovial fluid of 4 patients with reactive arthritis and 2 with ankylosing spondylitis.  CD8 cells were indeed found which killed Yersinia-infected HLA-B27 target cells in a patient with yersinia-induced reactive arthritis.  Similarly, salmonella-induced and yersinia-induced CD8 cells from one patient with salmonella-induced arthritis reacted with infected target cells.  In 5 of the 6 patients autoreactive CD8's were found, some of which demonstrated HLA-B27-restricted killing of uninfected cell lines

In killing uninfected target cells - true autoimmunity - the CD8 cells may have recognized a cross-reacting autologous peptide, created in some fashion by the presence of infected HLA-B27 cells.  By 1994, only a few of these peptides had been identified. Since that time more possibilities have surfaced, and the more recent concept of "frameshifting" of peptides in the MHC groove expands the possibility of T-cell confusion by an unknown, perhaps enormous factor.

Probst and colleagues found that a urease β-subunit of Yersinia enterocolitica produced CD8 T-lymphocyte stimulation, which added another possible peptide for HLA-B27 mimicry.  Patients with Guillian-Barre syndrome have demonstrated they have the polypeptide (ganglioside) GQ1b, which recognizes similar epitopes on specific Campylobacter jejuni strains of bacteria, which presents another peptide possibility [105].

If a peptide bound by HLA-B27 were the result of molecular mimicry between host and organism, the receptor site would be considered by the host to be "foreign".  This could easily explain autoimmunity, or the breaking of self-tolerance, since autoreactive cytotoxic CD8 cells could then continue to attack the HLA-peptide reaction site and persist, despite the absence of any initial triggering agent, such as bacteria, virus, etc.

            More recent research has been conducted which has shown the phenomenon of Th1-Th2 switching [42,76]. This is the ability, with antigenic stimulation, of a certain type of helper T-cell (Th1) to "switch" to another type of helper T-cell (Th2) that produces a different group of interleukins.  This may be the actual mechanism of production of the so-called T-suppressor cell.

            Even if CD8 T-cells are not fundamental to HLA-related mimicry, many other possibilities exist.  If indeed CD4 T-cells do proliferate in greater amounts than do CD8 T-cells, it is possible that the CD4 cell is produced as part of a defense mechanism to abrogate the effects of bacterial invasion, rather than being directly associated with mimicry at HLA-B27, HLA-DR4 or elsewhere.

Mimicry, the T-cell and EPD immunotherapy

            In 1966, Dr. Leonard M. McEwen, an immunologist in London, England, began development of a type of immunotherapy called Enzyme Potentiated Desensitization (EPD).  This immunotherapy has the ability to effectively desensitize patients to a wide variety of allergens and other agents to which a patient has somehow become allergic or "sensitized."  EPD employs several combinations (mixtures) of various antigens which may include pollens, molds, danders, foods, bacteria, chemicals and other antigens.  The principal differences between EPD and conventional immunotherapy is that the enzyme, β-glucuronidase, is added to the EPD mixture immediately before the injection is given, and the dosages used for EPD are very small.

β-glucuronidase appears to act as a lymphokine, which carries a "signal" via dendritic cells, to regional and systemic lymph nodes.  These lymph nodes are then induced to produce T-suppressor cells, generally over a period of about 36-48 hours, which have been specifically activated by the particular allergens administered with the β-glucuronidase.

            The role the CD8 "suppressor" cells selectively enhanced by EPD are postulated to play is to "suppress" CD4 T-cells which are "mis-calibrated", as these particular CD4 cells generally result in the production of allergy or intolerance in patients.

            EPD antigen mixtures are extremely dilute (approximately 10-14 to 10-6).  Treatment is generally given by intradermal injection into the skin of the forearm, which activated dendritic cells by way of the beta glucuronidase present, and is administered every two months at first, decreasing in frequency as time goes on.  Since T-cells have a relatively long half-life, many may survive in the circulation for several years, and many essentially live "forever".  The accumulated total number of "activated" or "immunized" T-cells produced by EPD treatment over time increases with each additional injection, and the immunotherapy may often be discontinued or decreased to very long intervals between injections (1 to 5 years or more).

            EPD immunotherapy has been employed by a significant number of physicians in the USA, Europe and a number of other countries.  Several studies have been conducted which have investigated the efficacy of EPD for various conditions.

            This author was the principal Investigator for a multi-center study of EPD immunotherapy.  Over a period of 10 years, the study group collected data for over 10,500 patients with highly variable disorders who have received EPD.  Additional material will be published from this outcome study.

            Given the knowledge that Proteus sp. and Klebsiella sp. play a major role in the etiology of rheumatoid arthritis and ankylosing spondylitis, McEwen developed a specific EPD bacterial antigen component, containing both Proteus and Klebsiella, called (P/K). At my request, McEwen also has produced a Bacteroides bacterial antigen, which I and several investigators employed in this study. We now have strep and Yersinia as well.

It is rather clear that EPD works by activating a type of CD8 T-cell.  Whether this type of T-cell is the direct cellular agent that mitigates arthritis (MHC class II), or whether it plays a role simply by suppressing activated CD4 cells (MHC class I) makes little difference in clinical outcome.

In the EPD study it was found that when patients who had illnesses historically associated with mimicry secondary to certain bacteria were treated with EPD (a T-cell-based immunotherapy), most improved considerably.  To me, this is in indication that the mimicry concept is valid, and that treatment with a specific vaccine is desirable.

When EPD became unavailable in 2002, LDA was developed for use in this country.  FDA-approved bacterial antigens are few and far between in this country, and since LDA was now compounded, and compounding pharmacies must purchase the material they use from FDA-approved suppliers, so the bacterial antigens McEwen used became unavailable.  I am able to tell other physicians how to legally procure and compound these bacterial allergens for LDA themselves, if they are interested and they are able to obtain the bacterial antigens from a laboratory themselves. Interestingly, the bacteria that cause the vast majority of bacterial-related autoimmune disease are present in a patient's stool. Some LDA physicians are now using autologous vaccines - vaccines made directly from the patient, used to treat those same patients. The effect has so far been at least 50% successful, better than we ever hoped.


It requires little stretch of the imagination to consider that perhaps most or all autoimmune disorders could be associated with interaction of organisms or even other substances with the body's MHC HLA-receptors.  It is likely that any or all of these interactions easily involve molecular mimicry. If that's the case, all one needs is the proper extract and dilution of the offending substance, mixed with a lymphokine like beta glucuronidase to actively treat the problem.

Although of limited availability due to the relatively small numbers of physicians who use them in the US, Canada and Europe, LDA and EPD immunotherapy both employ the principals of bacterial molecular mimicry to directly target T-cells and mitigate the adverse physical effects of rheumatoid arthritis, ankylosing spondylitis, most types of reactive arthritis and a growing list of other autoimmune disorders.


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