Hodgkin's disease as a failure of immune regulation: a re-interpretation of the epidemiological findings.

A failure of immune regulation has been often suspected as the basic condition leading to the development of Hodgkin's disease (HD), but the precise nature of this immune defects has not been defined. It is shown here that most of the epidemiological features fit the hypothesis of an increased risk for HD linked to an immune disbalance between a weak immune suppressor activity (ISA), and an enhanced polyclonal B cell activation (PBA). Few infections in childhood and an "untrained" immune system would lead to a weak ISA as the main risk factor among adolescent and young adults in the developed world, while an enhanced PBA due to chronic parasitic infections and malnutrition could explain a relatively high risk for HD among small children in undeveloped countries. The different histologic types of HD may reflect a variable contribution of a weak ISA, or an enhanced PBA under different conditions.