states of emergency and stress. The
situations when HSPs are most ex-
pressed, emergency and stress, are also
the ones where you may usually find
immune response. That alone suffices
to mark HSPs as useful examples to the
immune system, but more than that,
because states of emergency abound in
all environments, HSPs are essential
and are expressed in all cells. In fact,
these proteins are ubiquitous in cells in
times of stress and are highly preserved
throughout evolution, from prokaryotes
to multicellular organisms [19]. All this
suggests HSPs to be part of the useful
examples that build the achieved set
through which detection is carried out.
Now that we have proposed this pos-
sible achieved set (the homuncular an-
tigens), we can go on to the mechanism
of detection. If the immune system be-
haves according to our suggested
theory, we would expect several points
of immune behavior. We have just
shown that housekeeping genes in gen-
eral and HSPs in particular would be
good candidates as “useful examples,”
which would imply that the immune
system and its receptors would have a
bias in its reaction to these proteins
when reacting to the environment and
performing immune functions. At least
in HSPs this appears to be the case. Re-
ceptors to different types of endog-
enous and exogenous HSPs have been
shown to be important to immune re-
action. In Cohen and Young’s review of
the immunological reaction to HSPs,
they show that during almost any reac-
tion to bacteria and parasites, the rec-
ognized antigen detected is a type of
HSP [20]. In other immune activities, T
cells reactive to specific self-proteins,
for example, HSP60 and MBP (an essen-
tial factor in nervous tissue), have been
shown to enhance the regeneration of
skin and nerve tissue [21-24].
If the immune system is indeed
working as a cognitive system, as we
have described it, then the immune
mechanisms of detection should in-
clude a means for the detection of the
general properties of the environment
along with a mechanism for refitting to-
ward specific encounters. This should
allow for the deconstruction and recon-
struction of the immune “image.”
Therefore, we are expecting an adult
repertoire of receptors built to react de-
generately, at a median level of affinity,
to a few self-antigens. This repertoire
will not change much during our life-
time. Along side this, we expect a rep-
ertoire of non-self-reactive receptors,
which changes and evolves over time as
the immune system encounters patho-
gens and evolves throughout our life.
Both T cells and B cells have adult
receptor repertoires that are highly
cross-reactive and react degenerately to
self-antigens. These repertoires remain
at a steady level throughout life [13,25].
B cells have an added ability: when ac-
tivated by the innate immune reper-
toire, they start a process of fine tuning,
known as affinity maturation [26], by
which they create highly specific and
accurate receptors that react to a spe-
cific antigens. In B cells we find a sharp
distinction between a self-reactive rep-
ertoire, which remains permanent
throughout life, and a changing popu-
lation of receptors that is a result of the
immune system’s interactions with dif-
ferent immune events [25]. B cells,
while acquiring a growing repertoire
toward specific pathogens, during the
lifetime of the organism, maintain a
permanent repertoire of cross-reactive
receptors, possibly through inter-
action with the less changeable T-cell
repertoire.
The stability of T-cell repertoires and
fluidity of B-cell repertoires could very
well be a way to allow the process of
detection and refitting, while keeping
focused on the achieved set of molecular
life (homuncular antigens).
The existence of self-reactive recep-
tors does not mean that an autoim-
mune reaction of the immune system
is something that happens in health.
It means that such an occurrence
is avoided, not through the lack of
self-reactive immune receptors, but
rather through their heavily controlled
existence.
Although we have not described ex-
act cellular mechanisms of detection
and interaction, we feel that we have
given enough of an argument to justify
treating the immune system as a cogni-
tive system.
The immune system’s ability to
function is dependent on its under-
standing the environment in a cognitive
manner and its ability to discern the
complex patterns it encounters. The
world of immune function is the body
in which it resides. This is the source of
the examples it uses to see the generali-
ties of cellular life. These points imply a
new outlook at the receptor repertoire
of the immune system, which enables it
to react to changing and unexpected
patterns.
Our self is the source of examples,
and yet in the end the immune system
knows not to react to the patterns of
self. This could be because the immune
system has no receptors for self and so
the immune system can not “see” it. We
would suggest that this is not so, but
rather the immune system has many re-
ceptors with a sensitivity for self; how-
ever, their interaction is such that it rec-
ognizes the patterns of self as what they
are—the background on which the pic-
ture of immune events are painted. Self-
immunity is the basis not the nemesis
of immune function.
In closing, although we have used vi-
sion and language as examples to ex-
plain something about the immune
system, still in doing so we have also
put together principles that are at the
base of all cognitive systems. These
three systems are all different in their
particular components and in the spe-
cific fashion in which they interact with
their part of the environment. Still they
all share the common traits of dealing
with the specifics of their environment
through an acquired sensitivity to the
general properties of their environment.
We would say that this is what makes
them all cognitive systems.
Cognitive systems have the common
trait of functioning in an existing envi-
ronment constantly on the brink of
change. Noncognitive systems are built
with a limited hardwired perceptual
ability capable of reacting to certain
stimulants and no others. In cognitive
systems, the existence of a built in (ge-
netic) tendency promises the acquisi-
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CO M PLEXITY
© 2001 John Wiley & Sons, Inc.