Læknablaðið : fylgirit - 01.10.1980, Blaðsíða 16

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polyarthritis with symmetric, inflamma-
tory affection including joint and connec-
tive tissue involvement. Experimental dis-
eases of this type can be induced in several
ways, most often by subcutaneous or in-
tramuscular injection of selected tissue
components and/or microbial material in
oil-containing adjuvant — or even with
Freund’s adjuvant alone. However, all
known animal experimental models of this
type seem to lack important features as
compared to the typical ICTD in man, e.g.
presence of rheumatoid factor, self-perpe-
tuating capacity, extraarticular manifesta-
tions etc. But this type of experiment
shows, that immunizations with self or
not-self antigen applied in the organism as
a slow-turn-over antigen pool can induce
symmetric inflammatory synovitis, resemb-
ling one step in the pathogenesis of chronic
polyarthritis, probably due to immune-
complex induced type III inflammation.
In humans one experimental type of
ICTD is familiar, serumsickness. It may be
argued, that this disorder does not deserve
to be included with the ICTD's. However,
8—14 days after immunization with not-
self serum or protein, the patient develops
symptoms highly resembling ISTD: Fever,
malaise, arthralgia, synovitis, proteinuria,
hypertension, exanthema, urticaria or irido-
cyclitis. Apart from different antigens, the
pathogenesis is not very different from
that of rheumatic fever, and the clinical
symptoms closely resemble those associated
with streptococcal allergy. In these condi-
tions as well as in the animal experimental
polyarthritis the active course is self-limi-
ted. The tendency for self limitation in
these conditions is characteristic as com-
pared to the perpetuated course of “spon-
taneous” ICTD's.
A special and highly interesting animal
model of ICTD is known in the mouse: The
New Zealand black (NZB) mouse develops
with a high incidence a disseminated ICTD
with multiple signs of auto-immunization,
a clinical disorder closely resembling SLE
in man, and which takes a fatal course in
the mouse. The tendency to develop thi’s
disease is associated with the genetic equip-
ment of NZB-mice and studies on strains
of these mice have shown, that probably
this special animal-ICTD is etiologically
dependent on a virus infection. The study
of animal models with ICTDs, resembling
those occuring in man, can give valuable
information on pathogenetic mechanisms,
but since many ICTDs in man are also
closely linked to genetic factors, it is not
very probable that even extensive investi-
gation of animal ICTD can lead to any
definate conclusion concerning the exact
etiology and pathogenesis of any defined
ICTD in man. Parallel animal models, how-
ever, can illustrate pathogenetic possibili-
ties, and can help to describe selected im-
munobiological mechanisms of importance.
1. Patterns of clinical story in the indi-
vidual patient
The clinical story has always been of
high relevance, and has from old times
clearly showed, that ICTDs are indeed a
consequence of some previous happening,
e.g. streptococcal infection in rheumatic
fever etc. The clinical début and course can
be so obviously related to a streptococcal
infection, and it was very early recognized,
that specifically altered immunological re-
activity to strepthococcal membrane pro-
ducts was closely related to and perhaps
the cause of inflammatory reactions af-
fecting the whole mesenchymal space with
preference for synovial membranes, peri-
endo-myocardium, skin and central nervous
system. It is not very surprising that this
association between streptococcal infecti’on
and disseminated non-infectious disease
was rather early recognized, since immimo-
logy at the time was more or less syno-
nymous with the immunology of infection:
There was a clear correlation in time bet-
ween streptococcal infection and subse-
quent ICTD, the di'sease was often epi-
demic in character, the responsible micro-
organism and its traces in the form of
antibody were easy to demonstrate. Seve-
ral other ICTDs are associated with anam-
nestic infectious episodes in a similar way.
3. Clinical symptoms and signs
In the long previous era of medi’cine,
when immunology was mainly associated
with infectious disease, it was easy for the
clinician to assume that diseases with
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