Læknablaðið : fylgirit - 01.10.1980, Blaðsíða 25

19
their membrane an Fc-receptor, which can
bind to the Fc-part of the antigen-antibody
complex part of an immunoglobulin mole-
cule. When this happens on a cell mem-
brane, the K-lymphocyte, true to its name,
destroys the cell membrane and kills the
antigen-carrying target cell. Type II reac-
tions are very well described through ex-
planation of the pathogenic mechanism in
hemolytic anemia, in drug induced im-
munological damage to cells from blood
and bone marrow and from immunological
damage to other types of structured mem-
branes in the organism, for instance the
glomerular basement membrane or the al-
veolar basement membrane. Another clear
example of type II inflammatory damage is
known from the pathogenesis in Rhesus
disease of the newborn. It must be empha-
sized, that the specifi'c binding of antibody
to antigenic determinants incorporated in
cell membranes can impede cell functions
and decrease cell half life without involve-
ment of the complement system or K-
lymphocytes. Thus, the type II inflamma-
tory tissue damage is not obligately depen-
dent upon these two accessory mediating
systems.
If circulating antigen-antibody-complexes
can be found in blood and tissue fluid as-
sociated with a clinical condition, in which
immunopathogenesis is suspected, and if
the same antigen-antibody complexes as-
sociated with compement can be demon-
strated in the walls of blood vessels in in-
flamed tissue areas, there is a good reason
to belive that a type III immunological in-
flammatory reaction is involved in the pro-
cess (figure 3).
Type III reactions are very frequently
found in immunological tissue damage and
take part e.g. in the pathogenic process be-
hind rheumatoid arthritis, systemic lupus
erythematosus, polyarteritis nodosa, in-
fectious diseases, rheumatic fever, glomeru-
lonephritis and several others. If sufficient-
ly small, antigen-antibody complexes may
circulate in the blood without causing any
damage or any symptoms at all. And if
their size exceeds a certain limit they be-
come insoluble particles, which are phago-
cytized by monocytes or macrophages. The
size of an antigen-antibody complex deci-
des, whether the complex is apt to cause
immunological inflammati'on or not. The
size is determined by the concentrations of
antigen and antibody in plasma. The dan-
gerous size of antigen-antibody complexes
is achieved, when there is nearly equili-
brium between antigen and antibody with
a little surplus of antigen. Large, but still
soluble immune complexes with a sedi-
mentation constant of about 22 S are for-
med. These antigen-antibody complexes can
activate complement, endothelial cells be-
come stickly on their membranes, the mem-
brane permeability of the small blood
vessels is immensely increased, water and
dissolved material from the blood can filter
through the vascular walls with highly in-
creased speed, carrying with it also im-
mune complexes, complement and other
blood components. In the vascular wall,
however, the immune complexes are arres-
ted by membrane structures and further
conjugated to insoluble antigen-antibody
complexes, which are in their turn activa-
ting and binding the following links of the
complement chain. The inflammatory ef-
fects of complement factors C3a and C5a
TYPE III
_____________DAMAGE
Figure 3.