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Dr Alok Tripathi
Department of Biotechnology
aquaimmuno@yahoo.com
Hypersensitivities
• Immune responses to innocent antigens or
self antigens that lead to symptoms or tissue
damage
• Term “hypersensitivity” originally used to
denote acquired immune response, as was
“allergy”
• “Hypersensitivity” and Allergy” most
commonly refer to responses to innocent
antigens
• But autoimmune diseases are sometimes
subset of hypersensitivity
• Atopy is term used to describe condition of
general likelihood of responding with allergic
reaction
Classified by mechanism (Gel and Coombs 1963)
• Type I, Immediate: IgE antibody
triggering mast cells and eosinophils
• Type II, Antibody Mediated: IgG
antibody reacting with cell surface or
matrix antigens
• Type III, Immune Complex
Mediated: antigen-antibody
complexes
• Type IV: T cell mediated
Type I: allergies. IgE and mast
cells
Usefulness of “Type I” IgE responses:
eliminating parasites, like
helminths
Propulsive smooth muscle
contraction,
mucus prevent infiltration
of epithelium by parasites
About 20% of people in US have some form of allergy
• CD4 TH2 T cells
cytokine profile leads to
isotype switching to IgE
Sensitization
phase:
• IgE triggers Mast cell
degranulation
Effector
phase:
Sequence of events in Type I, “immediate
hypersensitivity”
Eosinophils & Basophiles contribute to the
chronic allergic reaction releasing similar
chemicals mediators to IgE binding to
FceeRI (which is induced in eosinophils by
inflammation)
 • Helper T cells (TH2) that secrete IL-4, IL-5, and
IL-13 are
 responsible for inducing allergen specific IgE
production
 • Non-atopic individuals also have T cells that
recognize
 allergens after sensitization, but in normal
individuals the
 T cells are kept in check by Tregs (IL-10 and TGFb)
 • Normal people activate TH1 helper T cells and
make IgG
 antibodies to same antigens
• Four distinct susceptibility genes
identified so far
– G-protein coupled receptor expressed in
inflamed tissue
8% of children under 3, 4% of US
adults Leading cause of
anaphylaxis outside of hospitals,
30,K ER cases per year
May lead to IgE or cell mediated
responses, and be expressed any
of atopic sites (gut, skin, bronchi,
systemic)
Gut largest immunologic organ
for Food allergy
•Systemic
antigen, like
bee sting
Systemic
response of
IgE cross
linking
receptors on
connective
tissue mast
cells and
circulating
basophils
• Desensitization with protein or peptide
antigens, with or without adjuvant
• Anti-IgE antibody
• – Xolair approved in 03 for asthma, but not yet
tested for peanut allergy (Genentech)
• – TNX-901 very effective in clinical trials but
removed
from testing by biotech squabbling
(Tanox/Genentech
legal battle)
• – Peanut allergy treated with
treated with peptide plusHeat
Killed Listeria, to induce TH1
response (in dogs, Frick 05)
• E.g., Ara
h 1,2, and 3
are peanut
proteins
• – Peptide epitopes recognized by
CD4 TCRs have been determined
• – Therapy with Fel d 1 peptides
increases TH1 T cellsrather then T
reg T cells (Alexander 05)
Fel d 1 is
component
of cat
dander
generation of
IgG antibodies
that prevent
allergic antigen
from reaching
IgE coated
mast cells
Desensitization may also be due to
Hygiene hypothesis
• Asthma and allergies increasing
dramatically in recent years in
developed countries
• Exposure to pathogens (larger
families, day care, farms) lowers
incidence of allergies
• Suggested that TH1 responses limit
TH2responses, but TH1 and TH2
are not solely antagonistic, and basis
of hygiene effects are notyet clear

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Introduction to Hypersensitivity & Allergy

  • 1. Dr Alok Tripathi Department of Biotechnology aquaimmuno@yahoo.com
  • 2. Hypersensitivities • Immune responses to innocent antigens or self antigens that lead to symptoms or tissue damage • Term “hypersensitivity” originally used to denote acquired immune response, as was “allergy” • “Hypersensitivity” and Allergy” most commonly refer to responses to innocent antigens • But autoimmune diseases are sometimes subset of hypersensitivity • Atopy is term used to describe condition of general likelihood of responding with allergic reaction
  • 3. Classified by mechanism (Gel and Coombs 1963) • Type I, Immediate: IgE antibody triggering mast cells and eosinophils • Type II, Antibody Mediated: IgG antibody reacting with cell surface or matrix antigens • Type III, Immune Complex Mediated: antigen-antibody complexes • Type IV: T cell mediated
  • 4. Type I: allergies. IgE and mast cells
  • 5. Usefulness of “Type I” IgE responses: eliminating parasites, like helminths Propulsive smooth muscle contraction, mucus prevent infiltration of epithelium by parasites
  • 6. About 20% of people in US have some form of allergy
  • 7.
  • 8.
  • 9. • CD4 TH2 T cells cytokine profile leads to isotype switching to IgE Sensitization phase: • IgE triggers Mast cell degranulation Effector phase:
  • 10.
  • 11. Sequence of events in Type I, “immediate hypersensitivity”
  • 12.
  • 13.
  • 14.
  • 15. Eosinophils & Basophiles contribute to the chronic allergic reaction releasing similar chemicals mediators to IgE binding to FceeRI (which is induced in eosinophils by inflammation)
  • 16.
  • 17.  • Helper T cells (TH2) that secrete IL-4, IL-5, and IL-13 are  responsible for inducing allergen specific IgE production  • Non-atopic individuals also have T cells that recognize  allergens after sensitization, but in normal individuals the  T cells are kept in check by Tregs (IL-10 and TGFb)  • Normal people activate TH1 helper T cells and make IgG  antibodies to same antigens
  • 18.
  • 19. • Four distinct susceptibility genes identified so far – G-protein coupled receptor expressed in inflamed tissue
  • 20. 8% of children under 3, 4% of US adults Leading cause of anaphylaxis outside of hospitals, 30,K ER cases per year May lead to IgE or cell mediated responses, and be expressed any of atopic sites (gut, skin, bronchi, systemic) Gut largest immunologic organ for Food allergy
  • 21. •Systemic antigen, like bee sting Systemic response of IgE cross linking receptors on connective tissue mast cells and circulating basophils
  • 22.
  • 23.
  • 24.
  • 25. • Desensitization with protein or peptide antigens, with or without adjuvant • Anti-IgE antibody • – Xolair approved in 03 for asthma, but not yet tested for peanut allergy (Genentech) • – TNX-901 very effective in clinical trials but removed from testing by biotech squabbling (Tanox/Genentech legal battle)
  • 26. • – Peanut allergy treated with treated with peptide plusHeat Killed Listeria, to induce TH1 response (in dogs, Frick 05) • E.g., Ara h 1,2, and 3 are peanut proteins • – Peptide epitopes recognized by CD4 TCRs have been determined • – Therapy with Fel d 1 peptides increases TH1 T cellsrather then T reg T cells (Alexander 05) Fel d 1 is component of cat dander
  • 27. generation of IgG antibodies that prevent allergic antigen from reaching IgE coated mast cells Desensitization may also be due to
  • 28. Hygiene hypothesis • Asthma and allergies increasing dramatically in recent years in developed countries • Exposure to pathogens (larger families, day care, farms) lowers incidence of allergies • Suggested that TH1 responses limit TH2responses, but TH1 and TH2 are not solely antagonistic, and basis of hygiene effects are notyet clear