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SEMINAR PRESENTED
ON
HYPERSENSITIVITY REACTIONS
SESSION: 2020-2021
PAPER-1
GUIDED BY PRESENTED BY-
ANKIT SHARMA
MSC. SEM 1
DEPARMENT OF BIOTECHNOLOGY & MICROBIOLOBY
RUNGTA COLLEGE OF SCIENCE AND TECHNOLOGY, GANJPARA, DURG (C.G)
RUNGTA COLLEGE OF SCIENCE &
TECHNOLOGY
PRESENTED BY:-
ANKIT SHARMA
M.Sc 1st sem
GUIDED BY :-
MISS S. SHWETA
• INTRODUCTION
• DEFINITION
• CLASSIFICATION
• TYPE OF HYPERSENSITIVITY
• MECHANISM
• CONCLUSION
• CURRENT RESEARCH
• REFERENCE
• Hypersensitivity (also called hypersensitivity reaction or intolerance)
refers to undesirable reactions produced by the normal immune
system, including allergies and autoimmunity.
• They are usually referred to as an over-reaction of the immune system
and these reactions may be damaging, uncomfortable, or occasionally
fatal.
• Hypersensitivity reactions require a pre-sensitized (immune) state of
the host.
• The Gell and Coombs classification of hypersensitivity is the most
widely used, and distinguishes four types of immune response which
result in bystander tissue damage
• Hypersensitivity reaction:- A condition in which the normally
protective immune system has a harmful effect on the body.
• Allergy:- An abnormal immunological response to an otherwise
harmless environmental stimulus (e.g., food, pollen, animal dander).
• “Hypersensitivity” generally represents the “dark side,” signifying the
undesirable aspects of an immune reaction, whereas the term
“immunity” implies a desirable effect.
• A hypersensitive response (HR) is an anti-pathogen response in plants
produced by avr-R system activation that leads to alterations in Ca+
flux, MAPK activation, and NO and ROI formation.
• There is rapid necrosis of plant cells in contact with the pathogen.
• This process prevents spread of the pathogen and releases hydrolytic
enzymes that facilitate injury to the pathogen’s structural integrity.
4 Types of HS (Gell & Coombs) :-
A. Type I: IgE-mediated degranulation of mast cells → acute
anaphylactic response ( Immediate hypersensitivity)
B. Type II: IgG / IgM on cells → c’ lysis or ADCC (Antibody- dependent
cytotoxic hypersensitivity)
C. Type III: Immune complexes → c’ activation, inflammation (Immune-
complex mediated cytotoxic hypersensitivity)
D. Type IV: TDTH activate macs → chronic inflammation (Delayed
hypersensitivity)
Note:- Types I – III involve Abs, Type IV is CMIR
• Commonly called allergy
• Mediated by IgE antibodies produced by plasma cells in response to
stimulation of Th2 cells by an antigens.
• The antigens that stimulate it are called allergens (i.e. House dust,
Pollens, Cosmetics, Insects, Clothing and Drug)
• Exposure may be ingested, inhalation, injection or direct contact.
• Type I hypersensitivity reactions can be systemic (e.g., systemic
anaphylaxis) or localized to a specific target tissue or organ (e.g.,
allergic rhinitis, asthma).
1. CLASSIC ALLERGIC REACTIONS -
• allergens – Ags that trigger HS-I reactions
• atopic people tend to mount IgE responses get hay fever, asthma,
etc.
2. MAST CELLS / BASOPHILS ARE MAJOR EFFECTORS -
• have high-affinity Fc receptors for IgE
• granules contain mediators of HS-I reaction
1. PRIMARY MEDIATORS IN MAST / BASO GRANULE-
• histamine
• serotonin- effects to histamine
• heparin- anticoagulant
• chemotactic factors recruit eos, neutrophils
2. SECONDARY MEDIATORS MADE LATER-
• arachadonic acid metabolites (PG, LT)
• platelet activ. factors (PAF)
• bradykinins
 LOCALIZED ANAPHYLAXIS (ATOPY)
• cutaneous anaphylaxis – wheal & flare
• (P-K Rx)
• urticaria
• allergic rhinitis (hay fever)
• food allergies
• atopic dermatitis (allergic eczema)
• asthma (lower resp. tract)
 SYSTEMIC ANAPHYLAXIS WORST CASE
• anaphylactic shock
• mast cells degran. all over body
• 3 potentially fatal Rx
• laryngeal edema – fluid leaking out → swelling
• bronchiole constriction → suffocation
• peripheral edema → shock from fluid loss
• 2° mediators cause prolonged effects later
• late phase reaction
• It is also known as antibody mediated cytotoxic hypersensitivity.
• Type II reaction occur when the antibody react with antigen determinants
present on the surface of cell leading to cell damage or death.
• Type II hypersensitivity involves IgG or IgM antibody-mediated.
• In these type of hypersensitivity occurs through the antibody dependent cell
mediated cytotoxic(ADCC).
• IgM or IgG immunoglobulin react with cell-surface antigens to activate the
complements system and produce direct damage of the sell surface.
• Transfusion reactions and hemolytic disease of the newborn are examples of
type II hypersensitivity.
• Type III hypersensitivity is also known as immune complex
hypersensitivity.
• The reaction may take 3 - 10 hours after exposure to the antigen (as in
Arhus reaction).
• The reaction may be general (e.g., serum sickness) or may involve
individual organs including or other organs.
• Generally it is due to antigen antibody complex.
• In these type of hypersensitivity reaction a complement system activated to
destroyed the target cell.
• Antigens causing immune complex mediated injury are:
i. Exogenous
ii. Endogenous
 LOCAL REACTIONS
 ARTHUS REACTION:
• It is named for Dr. Arthus.
• Inflammation caused by the deposition of immune complexes at a localized site.
• Clinical Manifestation is : Hypersensitivity Pneumonitis.
 SYSTEMATIC REACTIONS:
 SERUM SICKNESS:
• Systemic inflammatory response to deposited immune complexes at many areas
of body.
• Few days to 2 weeks after injection of foreign serum or drug it results in : Fever,
Urticaria, Artheralgia, Eosinophila, Spleenomegally, and Lymph adenopathy.
1) Hypersensitivity Pneumonitis
2) Glomerulonephritis
3) Rheumatoid Arthritis
4) Systemic Lupus Erythematosus.
• Inhalation of antigens into lungs stimulates antibody production.
• Subsequent inhalation of the same antigen results in formation of immune
complexes
 Activates complement.
GLOMERULONEPHRITIS
• Immune complexes in the blood are deposited in glomeruli
• Damage to the glomerular cells impedes blood filtration
• Kidney failure and, ultimately, death result
RHEUMATOID ARTHRITIS
• Immune complexes deposited in the joint
• Results in release of inflammatory chemicals
• The joints begin to break down and become distorted
• Trigger not well understood
• Treated with anti-inflammatory drugs
• Delayed hypersensitivity is a function of T Lymphocytes, not
antibody.
• It starts hours (or Days) after contact with the antigen and often
lasts for days.
• It can be transferred by immunologically committed (Sensitized) T
cells, not by serum.
• Principal pattern of immunologic response to variety of intra cellular
microbiologic agent
• i.e.: Mycobacterium Tuberculosis Viruses Fungi Parasites.
1. THE TUBERCULIN RESPONSE
• An injection of tuberculin beneath the skin causes reaction in individual
exposed to tuberculosis or tuberculosis vaccine
• Used to diagnose contact with antigens of M. tuberculosis
• No response when individual not infected or vaccinated
• Red, hard swelling develops in individuals previously infected or
immunized
• Cell-mediated immune response
• Results in an intensely irritating skin rash
• Triggered by chemically modified skin proteins that the body
regards as foreign Acellular, fluid-filled blisters develop in severe
cases
• Can be treated with glucocorticoids
ALLERGIC CONTACT DERMATITIS
COMPARISON OF DIFFERENT TYPES OF
HYPERSENSITIVITY:-
CONCLUSION :-
Hypersensitivity reactions are a result of either an immunologic
mechanism (allergic or anaphylactic reaction) generally mediated by
immunoglobulines E (IgE) or immunoglobulines G (IgG) antibodies
or a non immunologic mechanism (pseudo-allergic or anaphylactoid
reaction) related to different phenomenon such as non specific
histamine liberation.
CURRENT RESEARCH :-
• Hypersensitivity to biomedical implants: Prevention and
diagnosis.Rosner GA, Fonacier LS.Allergy Asthma Proc. 2017 May
1;38(3):177-183. doi: 10.2500/aap.2017.38.4052.PMID: 28441987
• Classification of hypersensitivity reactions.Dispenza MC.Allergy
Asthma Proc. 2019 Nov 1;40(6):470-473. doi:
10.2500/aap.2019.40.4274.PMID: 31690397
REFERENCE :-
• Kuby Janis, Immunology, 5th Edition, W.H. Freeman and company, New
York 2003(361-386) .
• Dulsy Fatima- Immunology, 1st Edition, Saras Publication 2009,(159-
181) .
• Moon TC, Befus AD, Kulka M (2014) Mast cell mediators: their
differential release and the secretory pathways involved. Front Immunol
5: 569.
• Coombs RRA (1992) The hypersensitivity reactions - some personal
reflections. Clinical and Experimental Allergy 22: 673-680.
• Kay AB (1997) Allergy and Allergic Diseases. Oxford: Blackwell
Science.
Paper 4 hypersensitivity

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Paper 4 hypersensitivity

  • 1. SEMINAR PRESENTED ON HYPERSENSITIVITY REACTIONS SESSION: 2020-2021 PAPER-1 GUIDED BY PRESENTED BY- ANKIT SHARMA MSC. SEM 1 DEPARMENT OF BIOTECHNOLOGY & MICROBIOLOBY RUNGTA COLLEGE OF SCIENCE AND TECHNOLOGY, GANJPARA, DURG (C.G)
  • 2. RUNGTA COLLEGE OF SCIENCE & TECHNOLOGY PRESENTED BY:- ANKIT SHARMA M.Sc 1st sem GUIDED BY :- MISS S. SHWETA
  • 3.
  • 4. • INTRODUCTION • DEFINITION • CLASSIFICATION • TYPE OF HYPERSENSITIVITY • MECHANISM • CONCLUSION • CURRENT RESEARCH • REFERENCE
  • 5. • Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity. • They are usually referred to as an over-reaction of the immune system and these reactions may be damaging, uncomfortable, or occasionally fatal. • Hypersensitivity reactions require a pre-sensitized (immune) state of the host. • The Gell and Coombs classification of hypersensitivity is the most widely used, and distinguishes four types of immune response which result in bystander tissue damage
  • 6. • Hypersensitivity reaction:- A condition in which the normally protective immune system has a harmful effect on the body. • Allergy:- An abnormal immunological response to an otherwise harmless environmental stimulus (e.g., food, pollen, animal dander). • “Hypersensitivity” generally represents the “dark side,” signifying the undesirable aspects of an immune reaction, whereas the term “immunity” implies a desirable effect. • A hypersensitive response (HR) is an anti-pathogen response in plants produced by avr-R system activation that leads to alterations in Ca+ flux, MAPK activation, and NO and ROI formation. • There is rapid necrosis of plant cells in contact with the pathogen. • This process prevents spread of the pathogen and releases hydrolytic enzymes that facilitate injury to the pathogen’s structural integrity.
  • 7. 4 Types of HS (Gell & Coombs) :- A. Type I: IgE-mediated degranulation of mast cells → acute anaphylactic response ( Immediate hypersensitivity) B. Type II: IgG / IgM on cells → c’ lysis or ADCC (Antibody- dependent cytotoxic hypersensitivity) C. Type III: Immune complexes → c’ activation, inflammation (Immune- complex mediated cytotoxic hypersensitivity) D. Type IV: TDTH activate macs → chronic inflammation (Delayed hypersensitivity) Note:- Types I – III involve Abs, Type IV is CMIR
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  • 10. • Commonly called allergy • Mediated by IgE antibodies produced by plasma cells in response to stimulation of Th2 cells by an antigens. • The antigens that stimulate it are called allergens (i.e. House dust, Pollens, Cosmetics, Insects, Clothing and Drug) • Exposure may be ingested, inhalation, injection or direct contact. • Type I hypersensitivity reactions can be systemic (e.g., systemic anaphylaxis) or localized to a specific target tissue or organ (e.g., allergic rhinitis, asthma).
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  • 14. 1. CLASSIC ALLERGIC REACTIONS - • allergens – Ags that trigger HS-I reactions • atopic people tend to mount IgE responses get hay fever, asthma, etc. 2. MAST CELLS / BASOPHILS ARE MAJOR EFFECTORS - • have high-affinity Fc receptors for IgE • granules contain mediators of HS-I reaction
  • 15. 1. PRIMARY MEDIATORS IN MAST / BASO GRANULE- • histamine • serotonin- effects to histamine • heparin- anticoagulant • chemotactic factors recruit eos, neutrophils 2. SECONDARY MEDIATORS MADE LATER- • arachadonic acid metabolites (PG, LT) • platelet activ. factors (PAF) • bradykinins
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  • 18.  LOCALIZED ANAPHYLAXIS (ATOPY) • cutaneous anaphylaxis – wheal & flare • (P-K Rx) • urticaria • allergic rhinitis (hay fever) • food allergies • atopic dermatitis (allergic eczema) • asthma (lower resp. tract)
  • 19.  SYSTEMIC ANAPHYLAXIS WORST CASE • anaphylactic shock • mast cells degran. all over body • 3 potentially fatal Rx • laryngeal edema – fluid leaking out → swelling • bronchiole constriction → suffocation • peripheral edema → shock from fluid loss • 2° mediators cause prolonged effects later • late phase reaction
  • 20. • It is also known as antibody mediated cytotoxic hypersensitivity. • Type II reaction occur when the antibody react with antigen determinants present on the surface of cell leading to cell damage or death. • Type II hypersensitivity involves IgG or IgM antibody-mediated. • In these type of hypersensitivity occurs through the antibody dependent cell mediated cytotoxic(ADCC). • IgM or IgG immunoglobulin react with cell-surface antigens to activate the complements system and produce direct damage of the sell surface. • Transfusion reactions and hemolytic disease of the newborn are examples of type II hypersensitivity.
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  • 23. • Type III hypersensitivity is also known as immune complex hypersensitivity. • The reaction may take 3 - 10 hours after exposure to the antigen (as in Arhus reaction). • The reaction may be general (e.g., serum sickness) or may involve individual organs including or other organs. • Generally it is due to antigen antibody complex. • In these type of hypersensitivity reaction a complement system activated to destroyed the target cell. • Antigens causing immune complex mediated injury are: i. Exogenous ii. Endogenous
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  • 25.  LOCAL REACTIONS  ARTHUS REACTION: • It is named for Dr. Arthus. • Inflammation caused by the deposition of immune complexes at a localized site. • Clinical Manifestation is : Hypersensitivity Pneumonitis.  SYSTEMATIC REACTIONS:  SERUM SICKNESS: • Systemic inflammatory response to deposited immune complexes at many areas of body. • Few days to 2 weeks after injection of foreign serum or drug it results in : Fever, Urticaria, Artheralgia, Eosinophila, Spleenomegally, and Lymph adenopathy.
  • 26. 1) Hypersensitivity Pneumonitis 2) Glomerulonephritis 3) Rheumatoid Arthritis 4) Systemic Lupus Erythematosus.
  • 27. • Inhalation of antigens into lungs stimulates antibody production. • Subsequent inhalation of the same antigen results in formation of immune complexes  Activates complement.
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  • 29. GLOMERULONEPHRITIS • Immune complexes in the blood are deposited in glomeruli • Damage to the glomerular cells impedes blood filtration • Kidney failure and, ultimately, death result
  • 30. RHEUMATOID ARTHRITIS • Immune complexes deposited in the joint • Results in release of inflammatory chemicals • The joints begin to break down and become distorted • Trigger not well understood • Treated with anti-inflammatory drugs
  • 31. • Delayed hypersensitivity is a function of T Lymphocytes, not antibody. • It starts hours (or Days) after contact with the antigen and often lasts for days. • It can be transferred by immunologically committed (Sensitized) T cells, not by serum. • Principal pattern of immunologic response to variety of intra cellular microbiologic agent • i.e.: Mycobacterium Tuberculosis Viruses Fungi Parasites.
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  • 33. 1. THE TUBERCULIN RESPONSE • An injection of tuberculin beneath the skin causes reaction in individual exposed to tuberculosis or tuberculosis vaccine • Used to diagnose contact with antigens of M. tuberculosis • No response when individual not infected or vaccinated • Red, hard swelling develops in individuals previously infected or immunized
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  • 35. • Cell-mediated immune response • Results in an intensely irritating skin rash • Triggered by chemically modified skin proteins that the body regards as foreign Acellular, fluid-filled blisters develop in severe cases • Can be treated with glucocorticoids
  • 37. COMPARISON OF DIFFERENT TYPES OF HYPERSENSITIVITY:-
  • 38. CONCLUSION :- Hypersensitivity reactions are a result of either an immunologic mechanism (allergic or anaphylactic reaction) generally mediated by immunoglobulines E (IgE) or immunoglobulines G (IgG) antibodies or a non immunologic mechanism (pseudo-allergic or anaphylactoid reaction) related to different phenomenon such as non specific histamine liberation.
  • 39. CURRENT RESEARCH :- • Hypersensitivity to biomedical implants: Prevention and diagnosis.Rosner GA, Fonacier LS.Allergy Asthma Proc. 2017 May 1;38(3):177-183. doi: 10.2500/aap.2017.38.4052.PMID: 28441987 • Classification of hypersensitivity reactions.Dispenza MC.Allergy Asthma Proc. 2019 Nov 1;40(6):470-473. doi: 10.2500/aap.2019.40.4274.PMID: 31690397
  • 40. REFERENCE :- • Kuby Janis, Immunology, 5th Edition, W.H. Freeman and company, New York 2003(361-386) . • Dulsy Fatima- Immunology, 1st Edition, Saras Publication 2009,(159- 181) . • Moon TC, Befus AD, Kulka M (2014) Mast cell mediators: their differential release and the secretory pathways involved. Front Immunol 5: 569. • Coombs RRA (1992) The hypersensitivity reactions - some personal reflections. Clinical and Experimental Allergy 22: 673-680. • Kay AB (1997) Allergy and Allergic Diseases. Oxford: Blackwell Science.