Arthritis Research

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We argue here that the risk of unresolved infection precipitating autoimmune disease is very low. The relevant information can be summarized as follows. First, there exists a group of "autoimmune" diseases, so designated because they fulfil (1) a set of generally accepted positive criteria, and (2) the negative criterion that reasonable efforts have failed to find an infectious causal agent. The group includes RA (rheumatoid arthritis), T1D (type 1 diabetes mellitus), MS (multiple sclerosis), and less frequent diseases such as MG (myasthenia gravis) and Graves' disease (thyroid autoimmunity). The positive criteria include presence of autoantibody and self-reactive T cells, immune pathology, MHC associations, and an animal model. Second, another group of diseases exists in which it is postulated that an infectious trigger establishes an autonomous, persistent immunopathology (damage caused by the immune system rather than the infectious agent on its own). This group includes ReA (reactive arthritis) and its related spondylarthropathies such as AS (ankylosing spondylitis), chronic rheumatic fever, Crohn's disease, Coxsackie virus-associated myocarditis, HSK (herpes simplex keratitis), antibiotic-resistant Lyme disease, and a number of tropical diseases [7, 97]. The question posed here concerns this latter group, and in particular whether the pathogen continues to drive the immunopathology in the later phase when the acute infection has subsided. Table 1 lists the evidence bearing on autoimmunity in these diseases.

We conclude from this survey that substantial efforts have so far failed to demonstrate that these infections can lead to self-sustaining autoimmu-nity. The main problem has been that although the disease typically lasts for years after the acute event, antigen derived from the infective agent, or the pathogen itself, remains detectable. Improved methods, notably PCR, have undermined the case for autoimmunity: Chagas' cardiac myopathy, for instance, has been subjected cogently to this critique [63]. Strikingly, in a mouse model of B3 coxsackievirus-associated myocarditis, CD4+ T cells themselves provide a source of the virus (M. Hesse et al., unpublished data), and in T1D the epidemiology has not convincingly demonstrated association with B4 coxsackievirus infection [50]. The main exception is AS, which we argue here may well represent a true instance of infection precipitating autoimmu-nity.

A discussion follows of two particularly informative diseases: Crohn's disease and AS. We present here a view of the chronic inflammatory diseases centred on immune dysregulation. Entering the two diseases in Table 1 as contradictory marks a difference, but does not exclude a connection between

communication communication the two. We argue that the neutrophil defect identified as causal in Crohn's disease can on occasion (depending on a genetic factor) allow enteric bacteria to trigger the autoimmunity of AS. We then show how recent advances in understanding immune downregulation have blurred the boundary between self and non-self, and how they strengthen the view that autoimmunity springs from immune dysregulation. Finally, we point out how misplaced fear of autoimmunity can hinder vaccine development.

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