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hygiene hypothesis
The hygiene hypothesis offers an explanation of why certain environmental exposures early in life may suppress or activate clinical disease.
      
The contribution of studies on parasites and allergy to our understanding of the hygiene hypothesis has been two-fold.
      
Parasitic infections are a major theme in the "hygiene hypothesis", as allergies and autoimmune diseases are less prevalent in countries with higher burdens of helminths and other parasitic organisms.
      
Parasitic infections are a major theme in the-"hygiene hypothesis", as allergies and autoimmune diseases are less prevalent in countries with higher burdens of helminths and other parasitic organisms.
      
-to: Gale EAM (2002) A missing link in the hygiene hypothesis Diabetologia 45:588-592
      
This contention also provides a suitable explanation for the 'hygiene hypothesis': infections re-enforce the physiological mechanisms of natural dominant tolerance, through the expansion of naturally occurring regulatory T cells.
      
It has been postulated that improvements in hygienic measures have led to an increase in allergic diseases ("hygiene hypothesis").
      
A substantial amount of research has been carried out to test the hygiene hypothesis.
      
Although the hygiene hypothesis might explain this in part, it is clear that it does not hold in all instances, and other factors are at work.
      
Another explanation which has gained much attention is the hygiene hypothesis.
      
Based on the hygiene hypothesis, bacterial infections could prevent or even treat allergic disease.
      
Circumstantial evidence is accumulating to support the extended hygiene hypothesis.
      
For every exposure studied with regard to the hygiene hypothesis, there are inconsistent findings in relation to asthma.
      
Hygiene hypothesis, suggesting the stimulation of TIM1 might directly regulate the development of Th2-biased immune response.
      
If this were indeed the case, it would add further support the so-called hygiene hypothesis.
      
In conclusion, bacterial components could be protective for asthma respiratory symptoms, which is in line with the hygiene hypothesis.
      
Mechanistic explanations for the hygiene hypothesis usually comprised a disbalance in Th1 and Th2.
      
Of these, only the hygiene hypothesis will be discussed in this thesis.
      
This review will examine recent epidemiologic studies of the hygiene hypothesis and asthma.
      
Therefore, other mechanisms must be taken into account as well to explain the hygiene hypothesis.
      
 

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