This document summarizes a seminar presentation on hypersensitivity reactions given by Ankit Sharma. The presentation covered the introduction, definition, classification, types, mechanisms and conclusion of hypersensitivity reactions. It discussed the four main types classified by Gell and Coombs, focusing on type I immediate hypersensitivity and allergic reactions. It provided examples of localized and systemic reactions, and the roles of mast cells, basophils, and primary and secondary mediators.

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

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

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).

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

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.

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

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.

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.

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

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

36. ALLERGIC CONTACT DERMATITIS

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.