Natural Autoimmunity

The existence of B and T-cells harboring self-reactivity complicates the concept of autoimmunity, since it goes to show that this property is not necessarily associated with disease states [18]. Moreover, the abundant existence of anti-self reactivity implies that representation of self within the immune system might even have teleological roles in terms of protection or immune modulation. As such, it has been initially proposed by Grabar [19] that natural autoantibodies (NAA) could act as transporters of catabolic products serving to clear the organism of harmful self as well as foreign substrates. This view has later been extended by suggesting that by low affinity binding to autoantigens, natural autoantobodies could function as filters preventing the induction of autoimmunity [20], An elaborate description of the biological roles of NAA is provided in Table 4.

A compelling theory regarding the essentials of this network has been proposed by I. Cohen designating the expression 'immunologic hommunculus'' to indicate the capacity of the brain to "imagine" itself.

NAA are bound to various structures found in the organism's body (i.e., serum proteins, cytokines and hormones) amongst which are also highly conserved self antigens (DNA, intracellular structures).

One of the unique properties of NAA is their independent production by the immune system, namely— they do not require antigenic stimuli as do other antibodies. NAA are predominately of the IgM isotype, although some consist of IgG and IgA. Another characteristic property is polyreactivity (widespread reactivity with infectious antigens and organic chemical substances).

The clinical significance of NAA has been questioned by some authors owing to their low avidities to self-antigens. Furthermore, the presence of NAA in huge amounts among patients with monoclonal gam-mopathies (Reference reviewed in [21]) without any corresponding clinical manifestations was inconsistent with a presumed pathogenic potential of these autoantibodies. This view was recently challenged by a set of studies in which active immunization with monoclonal antibodies (human IgM antibodies obtained from a healthy subject immunized with diphtheria and tetanus) resulted in the emergence of a clinical picture resembling human SLE and antiphospholipid syndrome [22].

Another relevant finding is the increased occurrence of NAA with ageing, which may seem paradoxical, owing to the well documented decline in immunologic functions accompanying the ageing process. Moreover, attempts to induce experimental autoimmune disease in aged animals are fraught with heightened resistance. Thus, the age-related increase in the incidence of autoantibodies can be considered a physiological process that improves the capacity of the individual to handle tissue damage.

NAA are probably produced by CD5 positive B-cells [23] by using selected unmutated germline genes that encode conserved sequences for large binding sites, capable of reacting with various autoantigens. This characteristic of NAA could explain the low affinities for different autoantigens.

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