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Artificial Immune Systems: a
new classifier
Andrew Watkins & Lois Boggess
Department of Computer Science
Mississippi State University
Metaphors from nature

Neural networks

Genetic algorithms
Biological immune systems
Pathogen
 Leucocytes

T cells (thymus)
 B cells (bone marrow)

Immune response
Pathogen
 Antigen presenting cells
 T cell (helper cell) and B cell
 B cell begins cloning and mutating
 Memory cells

T cells
B cells can’t “match” an antigen unless
a T cell does also
 Protection against self-destruction:

As T cells mature, those that match against
self are destroyed.
 Surviving T cells do not match self

Artificial Immune Systems

Some based on T cell analogy


(e.g., Dasgupta, University of Memphis,Forrest at
U.New Mexico)
Information Security






Example: data security
Data chopped into small segments
Lots of small random sequences from the alphabet of the
data
The ones that match are eliminated.
Rest recognize patterns not originally in the data
Can calculate how many needed on basis of alphabet and
acceptable risk of overlooking changes to data
Models based on B cells





Measure affinity of B cells to a presenting
antigen
The stronger the affinity, the more likely the B
cell is to change state and produce clones,
some of which are mutated
B cells that are not excited by antigens
eventually die
B cells “network” with similar B cells
Clusters visible in the results (e.g. Timmis et
al. and the Iris data)
Early work at MSU (Andrew
Watkins)
Used the B cell models
 Tried to modify to create a classifier
 Problem: B cells proliferated until a
system is swamped
 Problem: method for training the
classifier elusive

Resource limited AIS
Timmis’ group also had B cells swamping the
available computing resources
 Replace large numbers of identical B cells
with single representative (ARB) having a
resource number indicating “how many”
 Limit the total, and introduce competition

MSU contribution

Add class consciousness
Reward B cells which have strong affinity
to a presenting antigen of the same class
 At some point, also reward B cells which
have low affinity to antigens of different
class
 Take resources away from B cells which
respond inappropriately - eventually they
die

Training the memory cells
1
A
Memory Cell Pool
MCmatch
3
Mutated Offspring
2
4 A
5
MC candidate
ARB Pool
Effects of number of seed cells




Top two are accuracy
on training
Bottom two are
accuracy on test data
Slight trend toward
better accuracy with
more seed cells
Very different from
radial basis classifiers
Training algorithm
1. A training antigen is presented to all of the memory cells of
the same class as itself to find the memory cell MCmatch
2. MCmatch is added to the ARB pool along with its mutated
offspring; the number of offspring it is allowed to create
depends on the strength of the match
3. The training antigen is presented to the entire ARB pool. It is
at this point that we go through the stages of competing for
resources, culling the weakest ARBs, and producing mutated
offspring. This stage continues until the stimulation threshold
is met.
4. The strongest ARB of the same class as the training antigen
is chosen as the candidate memory cell. The strength of the
reaction of MCcandidate is compared with the strength of the
reaction of MCmatch to the training antigen.
Algorithm (cont.)
5.
If MCcandidate’s reaction is stronger than MCmatch’s
reaction then add MCcandidate to the Memory Cell Pool. If,
in addition to having this stronger reaction, MCcandidate is
closer to MCmatch than the product of the Affinity Threshold
and the Affinity Threshold Scalar, then replace MCmatch with
MCcandidate in the Memory Cell Pool.
Cleveland heart disease
Iris
IncNet
28-NN, stand, E uclid, 7
features
Fisher discrim inant
analysis
LDA
90.0
85.1
0.5
84.2
Grobian (rough)
SSV
100%
98.0%
3-NN + simplex
3-NN
98.7%
96.7%
Logdisc
IncNet
77.7%
77.6%
TAP MFT Bayesian
Na•ve MFT Bayesian
92.3%
90.4%
C-MLP2LN
98.0%
IB3
96.7%
DIPOL92
77.6%
SVM
90.4%
84.5
PVM 2 rules
98.0%
MLP + BP
96.0%
840.6
84.0
PVM 1 rule
AIRS
AIRS
C4.5
94.9%
94.9%
Best 2-lay er MLP + BP,
12 hidden
MLP+BP, 12 hidden
MLP+BP, 24 hidden
7
8
82.5-83.4
83.165
FuNe-I
NEFCLASS
97.3%
96.7
%
96.7%
96.7%
77.5%77.2%
76.8%
76.8%
90.4%
16-NN, stand, E uclid
FSM, 82.4-84% on test
only
Na•ve Bayes
AIRS
RIAC
SVM
94.6%
93.2%
76.6%
76.5%
1-NN, Manhatten
AIRS
84.2%
84.0%
9
SNB
83.1
CART
96.0%
92.0%
76.4%
MLP+BP, 6 hidden
83.5%
10
11
LVQ
kNN, k=27, M anh
FUNN
95.7%
92.8%
92.1%
LVQ
LFC
75.8%
75.8%
FSM - m ethodology?
1-NN Euclidean
83.6%
82.2%
12
13
GTO DT (5xCV)
kNN, k=19, E uclidean
82.9
82.8
0.6
82.5
82.10.8
Non-linear
perceptron
FSM + rotation
1-NN
Linear Discr.
Anal.
SMART
GTO DT
(5xCV)
ASI
Fischer discr.
anal
MLP+BP
DB-CART
Linear perceptron
91.3%
90.7%
RBF
NB
DB-CART, 10xCV
CART, 10xCV
81.8%
67.9%
14
LDA (all vectors, 85% on
train)
SVM (5xCV)
kNN (k=1?)
81.8
OC1 DT
89.5%
75.7%
75.573.8%
75.5%
81.5
81.5
CART
GTO DT
88.9%
86.0%
kNN, k=22,
Manh
MML
75.5%
SNB
75.4%
...
AIRS
74.1%
C4.5
73.0%
11 others reported with
lower scores, including
Bayes, Kohonen, kNN , ID3
Ι
1
2
3
4
5
6
15
16
Ι
22
23
others below 16th rank
include MLP with
Backprop, CART, RBF,
Gaussian EM, ASR, C4.5,
and a number of WEKA
tools, a mong others
Ionosphere
Diabetes
Sonar
84.7%
84.5%
We have only just begun

Lots of ideas for exploring the paradigm
 Andrew Watkins original ideas for modifications
 Don Goodman - exploring what happens when there
are lots of classes
 Gaurov Marwah - uniform probability assumed for
cloning and mutation - what if we introduce prob.
distributions?
 L. Boggess - nature doesn’t use pure mutation during
cloning process - what if we use some ideas from
sequence alignment to determine good mutation
sites?