Biology Reference
In-Depth Information
cooperate suicidally when selection would favor those that compete
successfully with conspecifics
crudely called “cheats?” In other words,
there should be a strong selective advantage for parents of infective larvae
to produce offspring that would defeat concomitant immunity and get
through to breed, even if that risks overcrowding the host. In the original
theoretical approaches to concomitant immunity, polymorphism in the
antigens or counter-immunity activities of invading larva had not been
considered.
68
Thus, it would be selectively advantageous to parents to
produce offspring that are different to others, resulting in the evolution of
polymorphisms in antigens. That would have the added effect of
increasing the genetic and antigenic diversity of those parasites that make
it through to adulthood because new incoming larvae that are antigeni-
cally similar to their predecessors will be selected against, thereby
favoring larvae that are different. Most nematode and schistosome
parasites reproduce sexually, so there is a mechanism for the evolution
and maintenance of high levels of polymorphisms within their
populations, just as is so evident in immunity genes in their hosts. See
69,70
for discussion of similar points for schistosomes based on infections with
parasites of differing known genotypes.
e
INN
ATE IMMUNITY AND COMPLEM
ENT
Protective immune responses against helminths such as Ascaris are
frequently attributed to Th2-dependent responses, IgE in particular. But
an observation made during a study that came to this conclusion also
found that inflammatory markers correlated with the development of
natural immunity in humans.
28
One such inflammatory-associated
response is complement, which is rarely investigated in nematode
infections (similarly with clotting). It has been established for a long time
that nematode surfaces can activate complement non-specifically through
the alternative pathway, and that their resistance to complement attack
could lie partly in their rapid shedding of surface materials.
71
e
74
It has
also been found that some nematode surfaces bind complement control
proteins that can disable activation of the full complement pathway and
consequent cellular inflammatory responses.
71,75
The complement system
in humans is highly polymorphic, and it could be that the apparent
differences in susceptibility in humans could be related in part to inher-
itance of differing complement alleles and their interactions.
Activation of innate responses also calls into mind pathogen-associated
patterns (PAMPs) that activate toll-like receptors (TLRs). The latter are
known to be activated by chemical signatures that are not present in
mammals (e.g. flagellin, LPS, mannan, bacterial lipoproteins) or genetic
material being present in an inappropriate compartment of cells (such as
