Page 64 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

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ing renal failure [RPGN]; → p.102ff.), while reaching its maximum effect in two to four
pulmonary involvement is characterized by days (delayed reaction type or delayed hyper-
life-threatening bleeding. sensitivity type [DHT]). It is triggered mainly
A type III reaction (→ B) is due to the forma- by proteins from pathogens (viruses, tuberculo-
tion and deposition of immune complexes (an- sis, lepra, bilharziasis, leishmaniasis, listerio-
tigen–antibody complexes), the antigens fre- sis, fungal infections), other foreign proteins
quently being connected to one another via (e.g., the wheat protein gliadin that causes ce-
the participating immunoglobulins (IgM, IgG). liac disease), and haptens, for example, drugs,
Such immune complexes not only activate the metals (e.g., nickel; → D), cosmetics, plant con-
complement system (→ p. 43, A1), but also stituents (e.g., pentdekacatechol in poison ivy
macrophages, granulocytes, and thrombocytes [Rhus radicans], or poison oak [Rhus toxicoden-
(via their Fc receptors). It is especially when dron]). Primary rejection of transplanted organs
the antigen is in excess that small, soluble im- is also a type IV reaction.
mune complexes circulate in blood for long pe- The antigen is phagocytized by macro-
riods (→ B, curves) and are only slowly broken phages, processed and presented to the (DHT-)
down. They are mainly deposited in the capil- T H cells (→ C). Sensitization takes more than
laries of the glomeruli (granular) but can also five days. On renewed contact, numerous
be found in joints, skin, and elsewhere. The T cells are activated into T H1 cells (→ p. 45ff.).
capillary wall will now be attacked by the These stimulate monocyte formation in bone
complement system as well as by phagocytes marrow via IL-3 and granulocyte-macrophage
Blood that have been chemotactically attracted and colony stimulating factor (GM-CSF), attract
monocytes and macrophages via chemokines,
then activated. The phagocytes liberate pro-
3 teases, oxidants, and inflammation mediators, e.g. MCPs (monocyte chemoattractant pro-
so that (immune complex) glomerulonephri- teins) and MIPs (macrophage inflammatory
tis, joint pains, urticaria, lymphadenitis, and proteins), activate them via interferon γ (IFN-
fever develop. These are symptoms that used γ) and with them (as well as with TNF-β) cause
to occur on passive immunization with vac- a strong inflammatory reaction in which en-
cines made from animal serum (cattle, sheep, dogenous or transplanted tissues may be ex-
horses) and were called serum sickness. tensively destroyed (tuberculosis, lepra, organ
A type III reaction can also be caused by in- rejection).
fections, if the immune system is unable to Often haptens on the skin are responsible
eliminate the pathogens completely (e.g., for a type IV reaction in the form of contact
streptococci or certain malaria protozoa), but dermatitis. Nickel in jewellery or watches can
enough antibodies are formed to maintain a get into the skin where, bound to endogenous
high concentration of immune complexes in protein, it is phagocytized as an antigen by the
the blood. Systemic lupus erythematodes is a skin macrophages (Langerhans cells) and pro-
type III reaction of unknown etiology. cessed (→ D). Subsequently, the macrophages
A local type III reaction can develop in the migrate to the regional lymph nodes and there
skin, for example, after vaccination (Arthus’ (after transformation to dendritic, B7-positive
phenomenon), or it can occur in the lung after cells) present the antigen to antigen-specific T
small amounts of antigen have been repeated- cells from the blood and lymph. The latter pro-
ly inhaled. On further contact, large amounts liferate and differentiate (to killer T cells and
of IgG are released (antigen excess) and com- T H1 cells) and in this way reach the site of anti-
plexes are formed that are precipitated in the gen exposure in large number (mainly via the
lung (exogenous allergic alveolitis). Examples blood; → C,D).
are bird fancier’s lung (antigens in bird excreta) Type V reactions are caused by autoanti-
and farmer’s lung (mold antigens in hay). bodies against transmitter receptors or hor-
A type IV reaction (→ C,D) is borne mainly mone receptors (→ p. 56).
by T H1 cells, killer T cells and macrophages,
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