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FIGURE 2.2 Hypothetical distribution of human genotypes involved in the
host eAscaris
relationships. Two groups of genes are considered: immune-related genes (i)
and genes influencing the susceptibility to parasite-induced immunomodulation (m). In the
atopic population immune-mediated resistance (iR) is supposed to be present, therefore,
variations in the genotypes depend on the resistance or susceptibility to immunomodula-
tion (mR and mS, respectively). In the non-atopic population, four genotypes may be pre-
dicted: iR/mR (underlying a high-resistant phenotype); iR/mS, iS/mR, and iS/mS, the
latter being present in the most susceptible subjects. The model assumes that the high-
resistance phenotype is not exclusive of the atopic population. Since several variants are
expected to occur in the genes of each genotype, in the general population the degree of
resistance/susceptibility will appear as a gradient. 49 Note that the separation of “i” and “m”
genes is done to get the simplest presentation of the hypothesis; however, this classification
is very artificial due to the difficulty in delimiting “immune-related genes” 161 and because
the immune response is just one component of the complex host e parasite interactions
during infection. Furthermore, “m” and “i” genes may have similar effect in terms of
defense.
from Ascaris , and have the lower levels of infection and better immunity.
Provided with the necessary environmental factors, they will have allergy
symptoms whether they are infected or not with Ascaris , and the infection
may increase symptoms. Other groups of allergy-prone individuals are
susceptible to immunomodulation; they will have more symptoms if
parasitic infections were removed. In addition, most of the population is
not predisposed to allergy, have variable immune-related resistance to
Ascaris , and variable susceptibility to helminth-induced immunomodu-
lation. Here the most typical forms of parasitic relationships will be
present; Ascaris control will have no effect on the prevalence of allergy in
this subpopulation.
The protective effect of allergy from ascariasis may have no great
individual clinical relevance, but it has potential epidemiological impact
and contributes to the analysis of the genetics of both allergy and Ascaris
resistance. For a long time it has been supposed that allergy is a legacy of
the evolutionary adaptive process of the protective response to helminths
and, as a consequence, genotypes associated with helminth resistance
are expected to be the same as those predisposing to allergy. Research
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