The innate immune system and its role in allergic disorders.
BACKGROUND
There has been an increasing prevalence of allergic diseases in the Western world over the last decades. The hygiene hypothesis has been proposed as a possible explanation for this epidemical trend in allergy. A key role in this theory is assigned to the reduced microbial stimulation of the Toll-like receptors (TLRs) in early life, which could lead to a weaker Th1 response and a stronger Th2 response to allergens. The individual immunological response is determined by the interplay between the dose and timing of exposure to endotoxins, other environmental factors and genetic predisposition. In the development and progression of allergic disorders, the innate immune system plays an important role.


OBJECTIVE
In this review, we discuss the paradoxical effects that may appear when the innate immune components are triggered. We review the influence of changes in the gene sequence and TLR expression in relation to the overall pattern of commensals and pathogens. We explored the possibility of alternative stimulations of the immune system by CpG oligodeoxynucleotides and probiotics as therapeutic devices against this endemic disease in Western society.


METHODS
Selection of papers was based on the importance of their contribution to the understanding of innate immunity and its implications.


CONCLUSIONS
The innate immune system plays an important role in both the protection against and the enhancement of allergic disorders, but the mechanisms are still unclear. Nevertheless, gene polymorphisms and triggers of the innate immune system provide therapeutic targets for protection against and treatment of allergic disorders.
Vandenbulcke
Liesbet
L
Upper Airways Research Laboratory, Department of Otorhinolaryngology, Ghent University, Ghent, Belgium. liesbet.vandenbulcke@ugent.be
Bachert
Claus
C
Van Cauwenberge
Paul
P
Claeys
Sofie
S
D006801:Humans; D006967:Hypersensitivity / Q000276:immunology* / Q000517:prevention & control*; D007113:Immunity, Innate / Q000187:drug effects* / Q000235:genetics*; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology