Purpose of review: Allergic and certain other inflammatory diseases have become more common in industrialized countries over the past few decades. One potential explanation for such trends is that with a decreased incidence of microbial exposures, as a result of modern public health practices, an important source of immune stimulation has been lost, with a consequent increase in inflammatory responses and their associated diseases. This review will focus on our current understanding of how microbial exposures impact on host immunity and the pathogenesis of allergic diseases.
Recent findings: In the past decade, it has become clear that a number of molecular interactions between immunocytes and microbial compounds are mediated by Toll-like receptors on host cells. Moreover, recent investigations have suggested that ligands for different Toll-like receptors have the potential both to inhibit and promote the development of allergic hypersensitivities and diseases.
Summary: On the basis of studies discussed herein, we speculate that physiological exposures to Toll-like receptor ligands have important yet complex effects on immune homeostasis and host susceptibility towards atopic diseases. Moreover, we anticipate that a fuller understanding of how physiological Toll-like receptor ligand exposures impact on immune development will lead to novel therapeutic interventions for the prevention and treatment of atopic diseases.