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Argued persuasively that because the pathologies differ the presence of sensitized T-cells is nonspecific and there are no disease-specific immune markers for MS; this is in fact a metabolic neurodegenerative disorder in which infectious agents(s) could be involved either in direct damage to the white matter or in inducing inflammatory responses that secondarily affect the brain (105). The evidence that MS is an autoimmune disease is indirect and based upon animal models (104). Different mechanisms suggested for disease initiation include epitope spreading, thymic dysregulation, and molecular mimicry, the latter based upon the hypothesis that microbial pathogens resemble human proteins and that exposure to these similar microbial epitopes may trigger an ‘‘auto’’ immune response against the host.

Many hypotheses regarding potential exogenous provokers of MS have been suggested, as discussed above and in Table 3, but almost all remain controversial. The defined but complex genetic interrelationships have defied interpretation and the conclusion can be drawn that a genetic predisposition appears to be a necessary (but not a sufficient) factor to confer susceptibility to MS. Further complicating the interpretation of the data, it is by no means certain that MS is a single disease entity (102); MS may represent a spectrum of disease.

81) Broadley et al. (168) Tosti et al. (166) Subgroup of patients with a first- or second- Annunziata et al. (173) degree relative with psoriasis had early MS onset Nielsen et al. 74)] No effect Vaccination Presence of ANA and antithyroid autoantibodies (ATAbs) No effect HB vaccination Danish study; 149,364 years of follow-up, but small numbers of events SS can mimic PPMS No significant differences in females, however Females only studied No need to modify vaccination regime See text Etiopathogenesis and Epidemiology: Clues to Etiology 21 22 Pryse-Phillips and Sloka Figure 5 Co-occurrence of multiple sclerosis with other diseases.

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