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Nutritional Immunology
Hypersensitivity/Allergy reactions
ROSHINA RABAIL
LECTURER, GOVERNMENT COLLEGE WOMEN UNIVERSITY, FAISALABAD, PAKIS TAN.
M.PHIL HUMAN NUTRITION AND DIETETICS
FORMER DIETITIAN CMH OKARA CANTT. & SHIFA INT. HOSPITAL ISLAMABAD
ROSHINA RABAIL 1
Hypersensitivity/Allergy reactions
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.
Such reactions are known as hypersensitivity reactions/allergy, and the
study of these is termed immunopathology.
An allergen is a substance that triggers an allergic reaction in people
who are sensitive to that substance.
Hypersensitivity refers to the undesirable or abnormal, sometimes fatal
immune reactions produced by the normal immune system. Results from:
Repeated exposure to an antigen/allergen
Response of adaptive immune system to self antigens (auto immune diseases)
ROSHINA RABAIL 2
Types of Hypersensitivity Reactions
Hypersensitivity reactions can be divided into four types: based on the
mechanisms involved and time taken for the reaction. (by R. Coombs and
P. Gell)
 (type I) Immediate hypersensitivity
 (type II) Antibody-mediated hypersensitivity
 (type III) Immune complex-mediated hypersensitivity
 (type IV) Cell-mediated hypersensitivity
Type V: (Autoimmune disease, receptor mediated) This is an additional
type that is sometimes (often in Britain) used as a distinction from Type 2.
ROSHINA RABAIL 3
ROSHINA RABAIL 4
Type I Hypersensitivity
Immediate or anaphylactic hypersensitivity and Commonly called Allergy
Occurs within minutes to the exposure to antigen
mediated by IgE, produced by plasma cells in response to T cells by antigens
IgE binds to mast cell or basophil causing them to result in degranulation and release
several mediators:
 Histamine: Increase permeability, mucous secretion and smooth muscle contraction
 Prostaglandins: Contraction of smooth muscles
 Leukotrienes: Bronchial spasms
Further reaction is amplified by platelets, neutrophils and eosinophils
Mast cells are triggered by some other stimuli such as:
exercise, emotional stress, Chemicals, anaphylotoxins
Anaphylactic Shock: Massive Drop in Blood Pressure, can be fatal in minutes
ROSHINA RABAIL 5
ROSHINA RABAIL 6
The HS I reaction may involve
skin (urticaria and eczema),
eyes (conjunctivitis),
nasopharynx (rhinorrhea, rhinitis),
bronchopulmonary tissues (asthma)
gastrointestinal tract (gastroenteritis).
Antigens that stimulate Type I HS are called Allergens
Examples are: House dust, pollens, cosmetics, Insects, Clothing, food, Drugs etc.
Three phases of Type I HS are: • IgE produced
by exposure
to allergen
Sensitization
• Next
encounter
with allergen
Activation
• degranulation
Effector
ROSHINA RABAIL 7
Type I Hypersensitivity
Anaphylactic shock
Anaphylaxis is a severe, whole-body allergic reaction to a chemicals that has become
an allergen.
This reaction is quick and involves the whole body.
Tissues in different parts of the body release histamine and other substances.
This causes the airways to tighten and leads to other symptoms.
Anaphylaxis can occur in response to any allergen. Common causes include:
 - Drug allergies
 - Food allergies
 - Insect bites/stings
ROSHINA RABAIL 8
Anaphylactic shock
Anaphylaxis is life-threatening and can occur at any time.
Risks include a history of any type of allergic reaction.
Symptoms:
develop rapidly, often within seconds or minutes. They may include the following:
Abdominal pain or cramping
Abnormal breathing sounds, wheezing, Difficulty breathing
Anxiety, Palpitations
Cough
Difficulty swallowing
Fainting, light-headedness, dizziness, Confusion
ROSHINA RABAIL 9
Type I HS Reactions
• Cutaneous anphylaxix
• Allergic rhinitis
• Food allergies
• Dermatitis
• Asthma
Localized
Anaphylaxis
• Anaphylactic Shock
• Mast cells degeneration all over body
• Laryngeal edema
• Bronchial constriction
Systemic
Anaphylaxis
ROSHINA RABAIL 10
Type I HS Reactions
ROSHINA RABAIL 11
Treatment
• Avoid Allergens
• Drugs:
◦ Anti-histamines: Compete histamine for its receptors
◦ Epinephrine : best for anaphylactic shock, (reverse effects of granules) quick but short
duration.
◦ Cortisone: Blocks histamine synthesis
Laboratory Tests for Type I Hypersensitivity
ROSHINA RABAIL 12
Type II Hypersensitivity
Cytotoxic
IgG or IgM antibody mediated
Involves complement system, phagocytes and T cells. Which directly damage cell
surface
The reaction time is minutes to hours.
Examples are:
Transfusion reactions: Incompatible donor cells are lysed
Haemolytic disease of newborn: Fetal cells are destroyed by maternal anti-Rh antibodies that cross the
placenta
Autoimmune haemolytic anemia resulted from drugs like Penicillin
ROSHINA RABAIL 13
Type III Hypersensitivity Reactions
Antigen Antibody immune complex hypersensitivity
3 - 10 hours after exposure to the antigen
Mediated by soluble immune complexes, IgG/IgM antibodies and
complement (C3a, 4a and 5a)
Large amounts of Antigen-Antibody complexes are accumulated in blood
When deposited in organs can cause inflammatory damages like:
Rheumatoid arthritis
Glomerulonephritis
ROSHINA RABAIL 14
The damage is caused by
platelets and neutrophils.
Diagnosis involves examination
of tissue biopsies for deposits of
immunoglobulin and complement
by immunofluorescence
microscopy
Examples are:
Serum Sickness from circulating
complexes e.g; Glomerulonephritis, RA,
Chronic infections
Arthus Reaction from localized
complexes e.g insect bite,
hypersensitivity pneumonitis
ROSHINA RABAIL 15
Type III Hypersensitivity Reactions
ROSHINA RABAIL 16
Arthus Reaction
ROSHINA RABAIL 17
Type III Hypersensitivity Reactions
Type IV Hypersensitivity
Delayed Hypersensitivity
T Cell mediated cytotoxicity
Start after hours to days of exposure
Release of cytokines, NK cells and macrophage activation
No antibodies involved
Localized reactions at site of antigen
Examples are: TB, Leprosy, Graft Rejection, contact dermatitis
ROSHINA RABAIL 18
Sensitization stage:
Memory T cells are generated by dendritic cells
Effector stage:
On secondary contact, T memory cells are activated and produce cytokines which cause
tissue destruction and inflammation
Continued exposure can cause chronic inflammation and result in granuloma formation
ROSHINA RABAIL 19
Type IV Hypersensitivity

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Hypersensitivity allergy reactions

  • 1. Nutritional Immunology Hypersensitivity/Allergy reactions ROSHINA RABAIL LECTURER, GOVERNMENT COLLEGE WOMEN UNIVERSITY, FAISALABAD, PAKIS TAN. M.PHIL HUMAN NUTRITION AND DIETETICS FORMER DIETITIAN CMH OKARA CANTT. & SHIFA INT. HOSPITAL ISLAMABAD ROSHINA RABAIL 1
  • 2. Hypersensitivity/Allergy reactions 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. Such reactions are known as hypersensitivity reactions/allergy, and the study of these is termed immunopathology. An allergen is a substance that triggers an allergic reaction in people who are sensitive to that substance. Hypersensitivity refers to the undesirable or abnormal, sometimes fatal immune reactions produced by the normal immune system. Results from: Repeated exposure to an antigen/allergen Response of adaptive immune system to self antigens (auto immune diseases) ROSHINA RABAIL 2
  • 3. Types of Hypersensitivity Reactions Hypersensitivity reactions can be divided into four types: based on the mechanisms involved and time taken for the reaction. (by R. Coombs and P. Gell)  (type I) Immediate hypersensitivity  (type II) Antibody-mediated hypersensitivity  (type III) Immune complex-mediated hypersensitivity  (type IV) Cell-mediated hypersensitivity Type V: (Autoimmune disease, receptor mediated) This is an additional type that is sometimes (often in Britain) used as a distinction from Type 2. ROSHINA RABAIL 3
  • 5. Type I Hypersensitivity Immediate or anaphylactic hypersensitivity and Commonly called Allergy Occurs within minutes to the exposure to antigen mediated by IgE, produced by plasma cells in response to T cells by antigens IgE binds to mast cell or basophil causing them to result in degranulation and release several mediators:  Histamine: Increase permeability, mucous secretion and smooth muscle contraction  Prostaglandins: Contraction of smooth muscles  Leukotrienes: Bronchial spasms Further reaction is amplified by platelets, neutrophils and eosinophils Mast cells are triggered by some other stimuli such as: exercise, emotional stress, Chemicals, anaphylotoxins Anaphylactic Shock: Massive Drop in Blood Pressure, can be fatal in minutes ROSHINA RABAIL 5
  • 7. The HS I reaction may involve skin (urticaria and eczema), eyes (conjunctivitis), nasopharynx (rhinorrhea, rhinitis), bronchopulmonary tissues (asthma) gastrointestinal tract (gastroenteritis). Antigens that stimulate Type I HS are called Allergens Examples are: House dust, pollens, cosmetics, Insects, Clothing, food, Drugs etc. Three phases of Type I HS are: • IgE produced by exposure to allergen Sensitization • Next encounter with allergen Activation • degranulation Effector ROSHINA RABAIL 7 Type I Hypersensitivity
  • 8. Anaphylactic shock Anaphylaxis is a severe, whole-body allergic reaction to a chemicals that has become an allergen. This reaction is quick and involves the whole body. Tissues in different parts of the body release histamine and other substances. This causes the airways to tighten and leads to other symptoms. Anaphylaxis can occur in response to any allergen. Common causes include:  - Drug allergies  - Food allergies  - Insect bites/stings ROSHINA RABAIL 8
  • 9. Anaphylactic shock Anaphylaxis is life-threatening and can occur at any time. Risks include a history of any type of allergic reaction. Symptoms: develop rapidly, often within seconds or minutes. They may include the following: Abdominal pain or cramping Abnormal breathing sounds, wheezing, Difficulty breathing Anxiety, Palpitations Cough Difficulty swallowing Fainting, light-headedness, dizziness, Confusion ROSHINA RABAIL 9
  • 10. Type I HS Reactions • Cutaneous anphylaxix • Allergic rhinitis • Food allergies • Dermatitis • Asthma Localized Anaphylaxis • Anaphylactic Shock • Mast cells degeneration all over body • Laryngeal edema • Bronchial constriction Systemic Anaphylaxis ROSHINA RABAIL 10
  • 11. Type I HS Reactions ROSHINA RABAIL 11 Treatment • Avoid Allergens • Drugs: ◦ Anti-histamines: Compete histamine for its receptors ◦ Epinephrine : best for anaphylactic shock, (reverse effects of granules) quick but short duration. ◦ Cortisone: Blocks histamine synthesis
  • 12. Laboratory Tests for Type I Hypersensitivity ROSHINA RABAIL 12
  • 13. Type II Hypersensitivity Cytotoxic IgG or IgM antibody mediated Involves complement system, phagocytes and T cells. Which directly damage cell surface The reaction time is minutes to hours. Examples are: Transfusion reactions: Incompatible donor cells are lysed Haemolytic disease of newborn: Fetal cells are destroyed by maternal anti-Rh antibodies that cross the placenta Autoimmune haemolytic anemia resulted from drugs like Penicillin ROSHINA RABAIL 13
  • 14. Type III Hypersensitivity Reactions Antigen Antibody immune complex hypersensitivity 3 - 10 hours after exposure to the antigen Mediated by soluble immune complexes, IgG/IgM antibodies and complement (C3a, 4a and 5a) Large amounts of Antigen-Antibody complexes are accumulated in blood When deposited in organs can cause inflammatory damages like: Rheumatoid arthritis Glomerulonephritis ROSHINA RABAIL 14
  • 15. The damage is caused by platelets and neutrophils. Diagnosis involves examination of tissue biopsies for deposits of immunoglobulin and complement by immunofluorescence microscopy Examples are: Serum Sickness from circulating complexes e.g; Glomerulonephritis, RA, Chronic infections Arthus Reaction from localized complexes e.g insect bite, hypersensitivity pneumonitis ROSHINA RABAIL 15 Type III Hypersensitivity Reactions
  • 17. ROSHINA RABAIL 17 Type III Hypersensitivity Reactions
  • 18. Type IV Hypersensitivity Delayed Hypersensitivity T Cell mediated cytotoxicity Start after hours to days of exposure Release of cytokines, NK cells and macrophage activation No antibodies involved Localized reactions at site of antigen Examples are: TB, Leprosy, Graft Rejection, contact dermatitis ROSHINA RABAIL 18
  • 19. Sensitization stage: Memory T cells are generated by dendritic cells Effector stage: On secondary contact, T memory cells are activated and produce cytokines which cause tissue destruction and inflammation Continued exposure can cause chronic inflammation and result in granuloma formation ROSHINA RABAIL 19 Type IV Hypersensitivity