Background The recent rise in the prevalence of immune-mediated diseases has been attributed to environmental factors such as a lack of microbial challenge, or dietary change, that deviate the overall balance between mutually antagonistic subsets of T helper (Th) cells.
Objective An alternative proposal is that recent environmental changes have resulted in an immune system that is more likely to produce both Th1 and Th 2 responses against benign antigens. The prediction of this hypothesis, that Th1 and Th 2-mediated diseases are not mutually exclusive, and may be positively associated, is tested here in a whole population.
Methods Data from General Practices participating in the Scottish Continuous Morbidity Recording (CMR) project were used to determine the coincidence of the major Th 2-mediated atopic diseases; asthma, eczema and allergic rhinitis, with the Th1-mediated autoimmune conditions; type I diabetes, rheumatoid arthritis and psoriasis. We also identified the prescription rates of inhaled therapy for asthma in patients with Th1-mediated disease.
Results There was a significant increase in the risk of presenting with a Th1-mediated autoimmune condition in patients with a history of allergic disease (standardized prevalence ratio (95% confidence interval) 1.28 (1.18–1.37)). Likewise, the standardized prevalence ratios of presenting with either eczema (1.67 (1.48–1.87)) or allergic rhinitis (1.22 (1.02–1.44)) were significantly increased in subjects with a history of Th1-mediated disease. There was a particularly strong association between current psoriasis and current eczema (standardized prevalence ratio of psoriasis in subjects with eczema 2.88, 95% confidence interval (CI) 2.38–3.45). There was also a significant increase in prescriptions for inhaled asthma therapy in patients with Th1 disease.
Conclusion It is concluded that Th1- and Th 2-mediated diseases are significantly associated in a large General Practice population. This finding supports the proposal that autoimmune and atopic diseases share risk factors that increase the propensity of the immune system to generate both Th1- and Th 2-mediated inappropriate responses to non-pathological antigens.