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people can present with chronic, high intensity infections with the adult
parasites yet without exhibiting disabling allergic manifestations in their
lungs or intestines. 18 It has been speculated that allergic manifestations of
hypersensitivity reactions, such as Loeffler's syndrome, are the conse-
quence of seasonal infections, in which hypersensitivity responses build
up during periods when transmission is not occurring, then are made
manifest when transmission resumes. 17,18 The assumption then is that
under conditions of continuous, low-level, trickle infections, humans do
not become hypersensitized and then respond adversely to migrating
larvae.
On considering Ascaris allergens, the one protein allergen that comes to
mind is ABA-1. This is one, if not the, major component of the pseudo-
coelomic fluid of adult worms, and is consequently the major protein in
allergen preparations (which tend to be crude extracts from adult worms)
used to test for allergic hypersensitivity to Ascaris. 21 e 24 ABA-1 is also
present in the larvae of Ascaris, although we could not find evidence that
the protein is synthesized either by tissue-migrating larvae during in vitro
culture, possibly because such culture conditions do not sufficiently
mimic conditions encountered by the larvae as they migrate (F. Qureshi
and M.W. Kennedy, unpublished), although cDNA encoding ABA-1 was
isolated from larvae. 25
While there are other proteins produced by Ascaris that are targets of
IgE responses in infections (and therefore, by definition, allergens), 26,27
ABA-1 will be a recurrent theme throughout the rest of this chapter
because of the detail now available on it from immune responses and
immunogenetics, to its molecular structure.
CORRELATION BETWEEN IGE ANTIBODY
TO ABA-1 AND ACQUIRED IMMUN ITY
One of the principal reasons for characterizing the antigens of parasitic
nematodes was the hope that naturally-acquired immunity could be
found to associate with reactivities to single or a small set of antigen types
in order to understand protective immunity and to identify protective
antigens for inclusion in vaccines. These ventures began in the 1980s, but
have met with limited if any success. One of the few examples in which
a correlation between immune reactivity (IgE antibody specifically) in
humans and naturally-acquired immunity was observed with ABA-1. 28,29
Even here, however, an effect was only observed with any confidence
when the study population was subselected for only those individuals
that reacted to the protein, excluding those that did not even if they
reacted to other antigens of the parasite (see below for immunogenetic
explanations for non-reactivity). 28 When infected people in Nigeria or
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