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HYPERSENSITIVITY
By,
Rajamehala M
What makes us sick?
“enemies” in the environment in the form of microbes and chemicals are
constantly attacking our bodies, disrupting homeostasis
sometimes immune system homeostasis is disrupted on its own
2
it may over-react to
antigens such as
with allergies
it may under-react as
with human
immunodeficiency
virus infection (HIV)
it may react to self
proteins as with
autoimmune disease
Hypersensitivity reaction
The immune system is an integral part of human protection against
disease, but the normally protective immune mechanisms can
sometimes cause detrimental reactions in the host.
Any immune response against a foreign antigen exaggerated beyond the
norm
Such reactions are known as hypersensitivity reactions, and the
study of these is termed immunopathology.
Gell & Coombs Classification
Type I:Immediate hypersensitivity
onset within minutes of antigen challenge
examples are allergies to molds, insect bites
Type II: Cytotoxic hypersensitivity
onset within minutes or a few hours of antigen challenge
examples are adult hemolytic anemia and drug allergies
Type III: Immune complex-mediated hypersensitivity
onset usually within 2-6 hours
examples include serum sickness and systemic lupus
Type IV: Delayed Hypersensitivity
inflammation by 2-6 hours; peaks by 24-48 hours
examples include poison ivy and chronic asthma
Type I (Anaphylactic) Reactions
Occur within minutes of exposure to antigen.
Antigens combine with IgE antibodies
IgE binds to mast cells and basophils, causing them to undergo
degranulation and release several mediators:
❖ Histamine:Dilates and increases permeability of blood vessels
(swelling and redness), increases mucus secretion (runny nose),
smooth muscle contraction (bronchi).
❖ Prostaglandins: Contraction of smooth muscle of respiratory
system and increased mucus secretion.
❖ Leukotrienes:Bronchial spasms.
Anaphylactic shock: Massive drop in blood pressure. Can be
fatal in minutes.
Biological basis of allergies
histamine
Type I hypersensitivity – sensitization to an inhaled allergen or bee sting
Antigens (red dots) from inhaled pollen are ingested and presented by
macrophages to T cells. Activated T cells produce cytokines leading to
the production of IgE, which binds to receptors on mast cells and causes
the release of histamine, which is responsible for allergy symptoms.
Onset is usually within minutes of contact with antigen.
Mast
cell
cytokines
→ →
Sensitization
•https://www.youtube.com/watch?v=uW96-mBFGag
Type II. Cytotoxic Type
Body makes special autoantibodies directed against self-cells
(antigens present on the surface of cells or other tissue
components)
antigen:
may be intrinsic to the cell membrane
may take the form of an exogenous antigen adsorbed on the
cell surface.
hypersensitivity results from the binding of antibodies to normal
or altered cell-surface antigens
Type II hypersensitivity – immune-mediated
destruction of red blood cells
Drug (p=penicillin) modified red blood
cells induce the production of
antibodies, because the bound drug
makes them look foreign to the immune
system. When these antibodies are
bound to them, the red blood cells are
more susceptible to lysis or
phagocytosis.
Onset is dependent on the presence of
specific antibodies.
Type II examples
1. Transfusion reactions
✔ cells from an incompatible donor react with the host’s antibody
2. Erythroblastosis fetalis
✔ there is an antigenic difference between the mother& the fetus, and
antibodies (IgG) cross the placenta & cause destruction of fetal red
cells.
3. Autoimmune hemolytic anemia, agranulocytosis, throbocytopenia
✔ individuals produce antibodies to their own blood cells, which are
then destroyed.
4. Drug reactions
✔ antibodies are produced that react with the drug.
https://www.youtube.com/watch?v=xllsDG2PXIk
Hypersensitivity Reactions

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Hypersentivity.pdf

  • 2.
  • 3. What makes us sick? “enemies” in the environment in the form of microbes and chemicals are constantly attacking our bodies, disrupting homeostasis sometimes immune system homeostasis is disrupted on its own 2 it may over-react to antigens such as with allergies it may under-react as with human immunodeficiency virus infection (HIV) it may react to self proteins as with autoimmune disease
  • 4.
  • 5. Hypersensitivity reaction The immune system is an integral part of human protection against disease, but the normally protective immune mechanisms can sometimes cause detrimental reactions in the host. Any immune response against a foreign antigen exaggerated beyond the norm Such reactions are known as hypersensitivity reactions, and the study of these is termed immunopathology.
  • 6. Gell & Coombs Classification Type I:Immediate hypersensitivity onset within minutes of antigen challenge examples are allergies to molds, insect bites Type II: Cytotoxic hypersensitivity onset within minutes or a few hours of antigen challenge examples are adult hemolytic anemia and drug allergies Type III: Immune complex-mediated hypersensitivity onset usually within 2-6 hours examples include serum sickness and systemic lupus Type IV: Delayed Hypersensitivity inflammation by 2-6 hours; peaks by 24-48 hours examples include poison ivy and chronic asthma
  • 7. Type I (Anaphylactic) Reactions Occur within minutes of exposure to antigen. Antigens combine with IgE antibodies IgE binds to mast cells and basophils, causing them to undergo degranulation and release several mediators: ❖ Histamine:Dilates and increases permeability of blood vessels (swelling and redness), increases mucus secretion (runny nose), smooth muscle contraction (bronchi). ❖ Prostaglandins: Contraction of smooth muscle of respiratory system and increased mucus secretion. ❖ Leukotrienes:Bronchial spasms. Anaphylactic shock: Massive drop in blood pressure. Can be fatal in minutes.
  • 8. Biological basis of allergies histamine
  • 9. Type I hypersensitivity – sensitization to an inhaled allergen or bee sting Antigens (red dots) from inhaled pollen are ingested and presented by macrophages to T cells. Activated T cells produce cytokines leading to the production of IgE, which binds to receptors on mast cells and causes the release of histamine, which is responsible for allergy symptoms. Onset is usually within minutes of contact with antigen. Mast cell cytokines → →
  • 11.
  • 12.
  • 13.
  • 14.
  • 16. Type II. Cytotoxic Type Body makes special autoantibodies directed against self-cells (antigens present on the surface of cells or other tissue components) antigen: may be intrinsic to the cell membrane may take the form of an exogenous antigen adsorbed on the cell surface. hypersensitivity results from the binding of antibodies to normal or altered cell-surface antigens
  • 17.
  • 18.
  • 19.
  • 20.
  • 21.
  • 22. Type II hypersensitivity – immune-mediated destruction of red blood cells Drug (p=penicillin) modified red blood cells induce the production of antibodies, because the bound drug makes them look foreign to the immune system. When these antibodies are bound to them, the red blood cells are more susceptible to lysis or phagocytosis. Onset is dependent on the presence of specific antibodies.
  • 23.
  • 24. Type II examples 1. Transfusion reactions ✔ cells from an incompatible donor react with the host’s antibody 2. Erythroblastosis fetalis ✔ there is an antigenic difference between the mother& the fetus, and antibodies (IgG) cross the placenta & cause destruction of fetal red cells. 3. Autoimmune hemolytic anemia, agranulocytosis, throbocytopenia ✔ individuals produce antibodies to their own blood cells, which are then destroyed. 4. Drug reactions ✔ antibodies are produced that react with the drug.
  • 25.