Hypersensitivity Type III

Cofreros, Renz Hadrien

MLS Intern
 Hypersensitivity Type III

• Characterized by tissue damage caused by the activation of

complement in response to antigen-antibody (immune)
complexes that are deposited in tissues.

• The classes of antibody involved are the same ones that

participate in type II reactions—IgG and IgM—but the
mechanism by which tissue damage is brought about is
different.
 Hypersensitivity Type III
• The consequences of antigen-and-antibody interaction within
the bloodstream vary according to whether the complexes
formed are large, in which case they are usually trapped and
removed by macrophages in the liver, spleen, and bone
marrow, or small, in which case they remain in the circulation.
 Large Complex
• Large complexes occur when
more than enough antibody is
present to bind to all the antigen
molecules.
• They form aggregates from many
antigen molecules cross-linked
together by the multiple binding
sites of IgG and IgM antibodies.
Small Complex
• Occurs when the ratio of antibody
to antigen is enough to form only
small complexes
• It causes the complement to
activate.
• the complexes tend to settle in
the narrow capillary vessels of
the synovial tissue, kidney and
skin
• The activation of complement leads to:
– increased permeability of the blood vessels
– release of histamine
– stickiness of platelets
– attraction of granulocytes and macrophages

• becomes more important when the antigen-antibody

complexes are deposited in blood vessels than when
they are deposited in the tissues outside the capillaries.
• The symptoms, depending on where the damage occurs, are
swollen, painful joints, a raised skin rash, nephritis (kidney damage,
causing blood proteins and even red blood cells to leak into the
urine), diminished blood flow to the brain, or gut spasms.

• The formation of troublesome antigen-antibody complexes in the

blood can also result from subacute bacterial endocarditis, a
chronic infection of damaged heart valves.
– The infectious agent is often Streptococcus viridans, normally a
harmless inhabitant of the mouth.
– The bacteria in the heart become covered with a layer of fibrin,
which protects them from destruction by granulocytes, while
they continue to release antigens into the circulation.