Dynamic load balancing is a form of load balancing that is more efficient in the face of incomplete
a priori information about task characteristics. In dynamic load balancing, the assignment of
tasks to processors (or agents) is done based on the current state of the system. Clearly, any load
balancing scheme based on the immune system metaphor will be dynamic.
Let us now examine each of the attributes of the immune system listed above and discuss their
application to load balancing.
The recognition capability of the immune system is a common requirement of computational
tasks. It is often the case that a program must carry out one or more searches for a given pattern.
In addition, the task usually requires that some action be carried out once the search has found
a target. In itself, recognition is not a process which serves load balancing ends. Rather, it
is a process which must itself be a target of load balancing processes. Nonetheless, recognition
processes, by their essentially parallel nature, put constraints on the load balancing processes. In
general, speeds for search operations scale linearly with the number of units engaged in the search,
and the immune system is no different in this regard. This does not mean, however, that the
optimal strategy is to employ all resources in the search activity and to redirect all these resources
to other activities once the target has been found. The system must be able to respond quickly to
unknown conditions, and assignment of all system resources to a given task may slow response to
some events.
Tolerance of “self-antigens” is crucial in the immune system, as otherwise the immune system
would attack everything in the body, and not limit itself to external invaders. In load balancing,
tolerance can be viewed as limiting irrelevant processing. That is, there may be environmental
conditions which signal or suggest that a certain computation should be done, but a computation
which does not contribute to the task being carried out. In this case the environmental condition,
or its signal, should be ignored, or tolerated, by the system. In the context of load balancing in
MIMD systems, the symptoms of the analog to an autoimmune disease would be the slowing down
of the rate in which problems are solved.
In the immune system tolerance is produced in a number of ways. The most well known is
that of clonal deletion, wherein a T-cell responsive to a self-antigen is killed in the thymus if it has
responded. This happens early in life, so there is a chance that self-antigens which appear later in
life (e.g. during puberty) will cause immune responses. For these case, the so-called peripheral T
cell tolerance mechanisms come into play. In peripheral tolerance, auto-immune responsive cells are
not killed but instead inactivated, a process referred to as anergy [15]. It is thought that anergy
results from a lack of proper co-stimulation of the cell. In co-stimulation, the presence of the
self-antigen must coincide with the presentation of B7 membrane proteins by Antigen Presenting
Cells (APCs) if there is to be an effective response. Anergy may also be caused if a variant form
of the antigen is encountered. Instead of anergy, tolerance can be mediated by suppression from
other lymphocytes (called suppressor T-cells). The mechanisms by which suppressor T-cells are
activated are similar to those thought to induce anergy. Anergy is not irreversible. The cytokine
IL-2 can cause anergic T cells to become reactivated.
The immune system employs a number of strategies for optimizing response speeds. One of
these is immunological memory [16]. When a given condition is first encountered, an effective
response to it may be slow in occuring. If a small number of units are henceforth dedicated to
detecting this specific condition, then future responses may be much faster. This is actually a load
balancing strategy as it dictates that a small number of agents be assigned to carry out a seemingly
irrelevant task in the hope that a rapid response can be attained when environmental conditions
change appropriately. In the immune system T-cells can either be “effector cells”, capable of taking
direct action against invaders, or “memory cells”. A recent theory of T-cell genesis [7] holds that
low antigen levels can cause young, naive, T-cells to become memory cells instead of effector cells.
In this case, then, environmental conditions can determine the function of a given agent. Another
theory [16] holds that effector T-cells become memory cells after a certain number of cell divisions.
In load balancing terms, this approach is saying that a T-cell that has undergone many divisions
in the past has done so in reponse to relevant environmental conditions, which are likely to arise
again in the future, even if they are currently not present.
An important way in which responses can be sped up is to use positive feedback. In the
immune system T4 “helper” cells stimulate themselves to reproduce through release of chemical
messages (proteins known as cytokines). Because of this positive feedback, the population of T4
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