OBJECTIVE: Many studies have examined the role of diet in the management of established rheumatoid arthritis (RA), warranting several recent reviews. However, none have considered the possible link between diet and the onset of RA in detail. Studies investigated a possible effect of individual components of diet and the development of RA, but the lack of a systematic review means there is no unbiased assessment of the evidence.

METHODS: We systematically reviewed studies with comparison groups that examined dietary intake or biological markers prior to the onset of RA. Four electronic databases were searched to identify relevant reports. Six quality criteria were agreed, against which the studies were assessed. The main outcome measure was a diagnosis of RA according to the ARA 1958 or revised ACR 1987 classification criteria.

Co-evolutionary development of the immune system together with infections and non-infectious environmental proteins (allergens) has generated biologically relevant thresholds and major directions to be taken by the immune system. The default healthy immune response to allergens is expected to be no response, however, detectable T cell and antibody (particularly IgG4 and IgG1) response has been demonstrated in sensitized, but clinically healthy individuals. If an immune response develops in healthy individuals, the immune system shows allergen-specific tolerance by using multiple mechanisms in order to keep the intensity of the inflammation low and tissue destruction small.

1,25-Dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) can modulate immune responses, but whether it directly affects B cell function is unknown. Patients with systemic lupus erythematosus, especially those with antinuclear Abs and increased disease activity, had decreased 1,25(OH)(2)D(3) levels, suggesting that vitamin D might play a role in regulating autoantibody production. To address this, we examined the effects of 1,25(OH)(2)D(3) on B cell responses and found that it inhibited the ongoing proliferation of activated B cells and induced their apoptosis, whereas initial cell division was unimpeded.

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