2. • Hypersensitivity can be defined as an
exaggerated response of the immune system
leading to host tissue damage
3. Plasma cells
• Plasma cells develop from B
lymphocytes (B cells), a type of
white blood cell that is made in
the bone marrow.
• Normally, when bacteria or
viruses enter the body, some of
the B cells will change into
plasma cells.
• The plasma cells make
antibodies to fight bacteria and
viruses, to stop infection and
disease. Enlarge
4.
5.
6. T-cells
• T cells express a receptor with the potential to
recognize diverse antigens from pathogens,
tumors, and the environment, and also
maintain immunological memory and self-
tolerance.
• T cells are also implicated as major drivers of
many inflammatory and autoimmune
diseases.
7.
8. Gell and Coombs’ classification
scheme
• On the basis of the highly influential Gell and
Coombs’ classification scheme, there are four
categories of hypersensitivity.
– Type I— immediate hypersensitivity
– Type II hypersensitivity - antibody-mediated
cytotoxicity.
– Type III hypersensitivity— complex-mediated
– Type IV hypersensitivity— cell-mediated.
9. Type I— immediate hypersensitivity
• anaphylactic or acute hypersensitivity
• IgE antibody
• mediated via degranulation of mast cells
leading to release of preformed factors
• promoting an influx of immune cells to the
site of mast cell activation and initiation of a
rapid inflammatory reaction.
10. • In the extreme case the inflammatory
response extends beyond the localized site of
initiation and affects systemic tissues leading
to life-threatening anaphylactic reactions
• Ex. Hay fever
11.
12. Type II hypersensitivity - antibody-
mediated cytotoxicity
• caused by antibodies that are directed against
cell surface antigens
• IgG and IgM are the key antibodies
13. • cytotoxic events would include activation of
the classical complement pathway leading to:
– formation of a MAC
– the attraction and activation of killing cells such as
NK cells or phagocytes
• Ex. blood transfusion reactions arising from
mismatch of the blood ABO antigens
14. Type III hypersensitivity— complex-
mediated
• formation of large antigen–antibody
complexes that circulate in the blood
• coated by complement proteins
• Removed by phagocytosis
– If this process is compromised for any reason then
the antigen–antibody complexes will be deposited
in tissue capillary beds
15. • This deposition of high molecular weight
antigen–antibody complexes in the glomerular
capillaries of the kidney can lead to a
condition termed glomerulonephritis which
involves disruption of the glomerular
basement membrane, destruction of
glomeruli and ultimately renal failure which
may necessitate organ transplantation.
16. • Systemic lupus erythematosus is a condition
where autoantibodies are directed against the
host’s DNA and RNA with subsequent
complement-coated immune complexes
deposited throughout systemic tissues such as
in the kidney, skin, joints and brain.
17.
18. Type IV hypersensitivity— cell-
mediated
• inappropriate accumulation of macrophages
at a localized site
• may or may not involve the presence of
antigen.
• Under conditions of ongoing localized
infection or inflammation, macrophages
release proteases, which destroy infected or
otherwise damaged tissue
19. • However, with the inappropriate recruitment
and/or activation of excessive numbers of
macrophages, continuing damage to normal
tissue may result, leading to chronic
inflammation.
• The recruitment and activation of macrophages
in type IV hypersensitivity is augmented by the
activity of helper T lymphocytes
• Ex. contact dermatitis
