POTENTIAL ROLE OF ENVIRONMENTAL FACTORS IN THE ETIOLOGY AND PATHOGENESIS OF ATOPY: A WORKING MODEL
 
   

Potential Role of Environmental Factors in
the Etiology and Pathogenesis of Atopy:
A Working Model

This section is compiled by Frank M. Painter, D.C.
Send all comments or additions to:
   Frankp@chiro.org
 
   

FROM:   Environ Health Perspect 1999;   107 Suppl 3 Jun:   485–7

Holt PG

TVW Telethon Institute for Child Health Research,
Perth, Western Australia.
patrick@ichr.uwa.edu.au


Sensitization to inhalant allergens commonly commences in utero, and most children are born with weak T helper–2 (Th2)–polarized T–cell immunity to these agents. During early life, these responses are normally deviated toward the Th1 cytokine profile. However, in atopics this immune deviation process fails, leading instead to consolidation of allergen–specific Th2 immunity and its eventual active expression in the airways. Both the induction and expression of Th2 immunity can be modulated by environmental agents that affect the cytokine milieu in the airway mucosa and/or the draining lymph nodes. Because of the known effects of the mold cell wall component (1-->3)-ss–d–glucan on monocyte cytokine secretion, exposure to molds during childhood may be a significant etiologic factor in allergic respiratory disease in general.


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