trans

306 HELMINTH SURFACES
schistosome tegument in immune evasion is
beyond the scope of this chapter. Instead, we
consider only a few examples that illustrate the
complex array of evasion strategies employed
by schistosomes to avoid destruction by natural
or vaccine-induced immune effectors. Compelling
evidence for the critical role of the tegument
in immune evasion comes from studies
showing that drugs that disrupt the outer
bilayer of the tegument, such as praziquantel
and oxamniquine, expose the parasite to extensive
damage from the host immune response.
Antisera that are toxic to schistosomes following
exposure to low concentrations of these compounds
have no intrinsic activity in the absence
of tegumental disruption. Several distinct physical
properties and proteins associated with
the tegument contribute to immune evasion
by schistosomes. However, definite evidence
that any one of them is more critical than others
is lacking. In this regard, several structural
features of the tegument may contribute to
immune evasion. The double membrane at the
apical surface of the tegument in schistosomes
may satisfy a structural requirement that allows
continuous replacement of old or immunologically
damaged membrane by new membrane
derived from the multilaminate vesicles. The
double membrane may also permit host antigens,
largely blood group glycolipids and glycoproteins,
to be incorporated into the surface of
the parasite, thereby disguising it from immune
attack. This form of camouflage is supplemented
by another form, commonly referred to
as molecular mimicry, wherein parasite-derived
molecules that contain host-like epitopes are
exposed at the surface. These proteins include,
for example, homologs of the Na -dependent
glucose transporter SLGT1, which are abundantly
expressed on the surface of the apical
tegumental membrane in schistosomes and
fasciolids (see below). Some lipid components
of this membrane, such as lysophosphatidyl
choline, also protect the organism by lysing
attached host leukocytes. Parasite-derived
enzymes capable of degrading host proteins,
including the cysteine protease SmCL1, are
present at high levels on the surface. Some may
be able to degrade host immunoglobulins.
Paradoxically, the tegument of schistosomes
also contains numerous proteins and glycoproteins
that are potent immunogens. Several of
these proteins, including the glycolytic enzymes
glyceraldehyde-3P-dehydrogenase and triosephosphate
dehydrogenase, are released from
the tegument and appear to play a role in concomitant
immunity to reinfection (i.e. they
stimulate production of antibodies that bind to
schistosomula in subsequent infections).
Nutrient absorption
A role for the tegument in nutrient absorption
can be inferred on the basis of structural,
biochemical and ecological considerations.
Numerous pits and channels provide an enormous
surface area for absorption, and the tegument
in adult stages is continuously exposed
to host fluids, from which the parasite derives
all of its nutrients. Several enzymes that function
in amino acid absorption are located in
the tegument, and in some cases (e.g. leucine
aminopeptidase), these enzymes are absent
from the intestine. Both S. mansoni and
F. hepatica can survive extended in vitro incubations
in the absence of detectable nutrient
absorption across the gastrodermis. In addition,
glucose absorption occurs in immature
stages of trematodes, which lack an intestine.
Adult schistosomes are absolutely dependent
on host serum glucose for energy. Glucose
flux across the tegument occurs by an active,
Na -dependent, carrier-mediated process. The
inward-directed Na gradient is maintained,
in part, by at least one Na /K -ATPase in the
tegument. This provides part of the electrochemical
driving force for hexose transport.
BIOCHEMISTRY AND CELL BIOLOGY: HELMINTHS