Page 92 - Textbook of Pathology, 6th Edition

76 Local anaphylaxis: iv) Idiopathic thrombocytopenic purpura (ITP) is the
i) Hay fever (seasonal allergic rhinitis) due to pollen immunologic destruction of platelets by autoantibodies
sensitisation of conjunctiva and nasal passages. reacting with surface components of normal plaletets.
ii) Bronchial asthma due to allergy to inhaled allergens like v) Leucopenia with agranulocytosis may be caused by
house dust. autoantibodies to leucocytes causing their destruction.
iii) Food allergy to ingested allergens like fish, cow’s milk, vi) Drug-induced cytotoxic antibodies are formed in response
eggs etc. to administration of certain drugs like penicillin, methyl
iv) Cutaneous anaphylaxis due to contact of antigen with dopa, rifampicin etc. The drugs or their metabolites act as
skin characterised by urticaria, wheal and flare. haptens binding to the surface of blood cells to which the
SECTION I
v) Angioedema, an autosomal dominant inherited disorder antibodies combine, bringing about destruction of cells.
characterised by laryngeal oedema, oedema of eyelids, lips, 2. Cytotoxic antibodies to tissue components. Cellular
tongue and trunk. injury may be brought about by autoantibodies reacting with
some components of tissue cells in certain diseases.
Type II: Cytotoxic (Cytolytic) Reaction
i) In Graves’ disease (primary hyperthyroidism), thyroid
Type II or cytotoxic reaction is defined as reactions by autoantibody is formed which reacts with the TSH receptor
humoral antibodies that attack cell surface antigens on the to cause hyperfunction and proliferation.
specific cells and tissues and cause lysis of target cells. Type ii) In myasthenia gravis, antibody to acetylcholine receptors
II reaction too appears generally within 15-30 minutes after of skeletal muscle is formed which blocks the neuromuscular
exposure to antigen but in myasthenia gravis and thyroiditis transmission at the motor end-plate, resulting in muscle
it may appear after longer duration. weakness.
ETIOLOGY AND PATHOGENESIS. In general, type II iii) In male sterility, antisperm antibody is formed which
reactions have participation by complement system, tissue reacts with spermatozoa and causes impaired motility as well
macrophages, platelets, natural killer cells, neutrophils as cellular injury.
and eosinophils while main antibodies are IgG and IgM. iv) In type 1 diabetes mellitus, islet cell autoantibodies are
Type II hypersensitivity is tissue-specific and reaction formed which react against islet cell tissue.
occurs after antibodies bind to tissue specific antigens, v) In hyperacute rejection reaction, antibodies are formed
most often on blood cells. The mechanism involved is as against donor antigen.
under (Fig. 4.7, B):
i) The antigen on the surface of target cell (foreign cell) Type III: Immune Complex Mediated (Arthus) Reaction
General Pathology and Basic Techniques
attracts and binds Fab portion of the antibody (IgG or IgM) Type III reactions result from deposition of antigen-antibody
forming antigen-antibody complex. complexes on tissues, which is followed by activation of the
ii) The unattached Fc fragment of antibodies (IgG or IgM) complement system and inflammatory reaction, resulting in
forms a link between the antigen and complement. cell injury. The onset of type III reaction takes place about 6
iii) The antigen-antibody binding with Fc forming a link hours after exposure to the antigen.
causes activation of classical pathway of serum complement ETIOLOGY. Type III reaction is not tissue specific and occurs
which generates activated complement component, C3b, by when antigen-antibody complexes fail to get removed by the
splitting C4 and C2 by C1. body’s immune system. There can be 3 types of possible
iv) Activated C3b bound to the target cell acts as an opsonin etiologic factors precipitating type III reaction:
and attracts phagocytes to the site of cell injury and initiates
phagocytosis. 1. Persistence of low-grade microbial infection. A low-
v) Antigen-antibody complex also activates complement grade infection with bacteria or viruses stimulates a
system and exposes membrane attack complex (MAC) that somewhat weak antibody response. Persistence of infection
attacks and destroys the target cell. (antigen) and corresponding weak antibody response leads
to chronic antigen-antibody complex formation. Since these
EXAMPLES OF TYPE II REACTION. Examples of type II complexes fail to get eliminated from body fluids, they are
reaction are mainly on blood cells and some other body cells instead deposited in tissues e.g. in blood vessel wall,
and tissues. glomeruli, joint tissue etc.
Cytotoxic antibodies to blood cells. Most common examples 2. Extrinsic environmental antigen. Exogenous antigens
of type II reaction are on blood cells. may be inhaled into the lungs e.g. antigens derived from
i) Autoimmune haemolytic anaemia in which the red cell injury moulds, plants or animals. The inhaled antigen combines
is brought about by autoantibodies reacting with antigens with antibody in the alveolar fluid and forms antigen-
present on red cell membrane. Antiglobulin test (direct antibody complex which is deposited in the alveolar walls.
Coombs’ test) is employed to detect the antibody on red cell 3. Autoimmune process. Another sequence in type III
surface (Chapter 12). reaction can be formation of autoantibodies against own
ii) Transfusion reactions due to incompatible or mismatched tissue (self antigen) forming autoantibody-self antigen
blood transfusion. complex. Such self antigens can be circulating (e.g. IgA) or
iii) Haemolytic disease of the newborn (erythroblastosis tissue derived (e.g. DNA). Immune complexes containing
foetalis) in which the foetal red cells are destroyed by maternal both components from body’s own system can thus be
isoantibodies crossing the placenta. deposited in tissues.