Phytotherapy for autoimmune disease: a focus on multiple sclerosis

Townsend Letter for Doctors and Patients,  May, 2004  by Kerry Bone

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Introduction

In a previous article published in the Townsend Letter I described an innovative multifactorial model for the development of autoimmune disease. (1) The implications of this model in terms of selecting herbal treatments were also discussed. The model, which can be described as a dual signal hypothesis, proposes two basic simultaneous requirements for the development of autoimmune disease. These are the primary lesion (the driver behind the attack on self which determines the site of the autoimmune reaction) and a state of immune dysregulation (an abnormal responsiveness of the immune system in some compartments). In particular, the role of micro-organisms in the onset and progression of autoimmune disease was stressed.

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An essential feature of this model is that the capacity for self-recognition is a normal immune function. In other words, immune cells which could cause autoimmune disease exist in every normal individual. The capacity for self-recognition, and indeed autoimmune response, may serve a useful function when controlled by appropriate regulatory factors, for example dead tissue clearance and stimulation of healing. This has certainly been proposed in the context of multiple sclerosis (MS). (2)

The following quotation is from a review article entitled "Tolerance and Autoimmunity" which was published in the New England Journal of Medicine in 2001 (3): "Since immunization of normal animals with certain self-antigens in an adjuvant induces autoimmune diseases, it follows that autoreactive T cells must be present in normal animals. Indeed, B cells and T cells that recognize insulin or myelin basic protein can be isolated from persons without diabetes or multiple sclerosis, respectively....

"Considerable evidence implicates infection as a cause of autoimmune diseases, such as multiple sclerosis and type 1 diabetes. Mechanisms that could lead from infection to autoimmunity include the release of sequestered autoantigens through tissue damage, the activation of a large fraction of the T-cell population by superantigens, and the induction of inflammatory cytokines and costimulatory molecules by microbial products. In mice, so-called bystander activation of this type can precipitate autoimmune diabetes.

"Alternatively, a structural similarity between microbial and self-antigens ("molecular mimicry") could have a key role in activating autoreactive T cells. Indeed, some T cells can recognize both a microbial peptide and a self-peptide with a similar amino acid sequence."

With the proposed model, many event sequences are possible. The simplest example is that the same micro-organism acts as both the primary lesion and the source of immune dysregulation. This may be the case for the autoimmune destruction which can occur with HIV-1 infection. In another scenario, a person might already be in a state of immune dysregulation and then react inappropriately to an infection. The infection passes, but the state of immune dysregulation persists and, because of the influence of the infection, develops into a self-sustaining autoimmune process. In this instance, best results will be achieved by concentrating treatment on the immune dysregulation and the self-sustaining inflammatory processes.

Another possible event sequence is that there is a chronic presence of a micro-organism to which the immune system is responding in a normal way. However due to molecular mimicry the micro-organism is also inducing a cross-reaction with self tissue. But this cross-reaction only occurs to a mild, non-damaging degree because the immune system is behaving normally. (This could also include a potentially pathogenic organism in the bowel flora.) Other events then trigger a state of immune dysregulation and the immune system begins to aggressively cross-react and destroy self tissue. In this instance, both the primary lesion (the micro-organism presence) and the cause of immune dysregulation require equal attention.

Another variation is possible which could be relevant to the development of MS. Here, at a certain age, a viral infection creates a clone of T lymphocytes which are capable of cross-reacting with self tissue. However, because there is no immune dysregulation, no damaging cross-reaction occurs, but these cells persist as memory cells after the virus has gone. They are then reactivated by exposure to the same virus, or one that is antigenically similar. If this event coincides with a state of immune dysregulation, autoimmune disease may develop. In this example the best approach to treatment is to (1) prevent the potential triggering effect of the second viral exposure or infection and (2) decrease the immune dysregulation and self-sustaining inflammatory processes.

The involvement of micro-organisms in the development of autoimmune disease is a controversial and confusing issue. Because an autoimmune disease is not an infection, but rather might be an abnormal response to micro-organisms under particular circumstances, it would be unreasonable to expect a single species of micro-organism only to be implicated in each autoimmune disease. This makes an "infectious" etiology difficult to prove, particularly if the implicated micro-organisms vary from region to region and from person to person. As might be expected from the model, studies in the current scientific literature have implicated the association of several micro-organisms with each autoimmune disease. These can provide useful information and will be reviewed below in the context of MS.