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Allergy

Hypersensitivity, or excessive immune response, can be classified into four main types. Type I is an immediate, IgE-mediated allergy. Type II involves antibodies attacking the body's own cells. Type III occurs when large amounts of antigen-antibody complexes are formed and deposited in tissues, activating complement and causing inflammation. Type IV is a cell-mediated response involving T cells and cytokines that cause tissue damage. The four types have different mechanisms but commonly involve an overactive immune response causing harm.

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Topic: 'Hyper sensitivity' Presented by: Sadya Laraib 6th semester (A) Roll no. 30.
1. Definition:  It is excessive immune response which leads to undesirable consequences, i.e. tissue or organ damage/ dysfunction.  immune responses which are damaging rather than helpful to the host.  Excessive immune response in a sensitized individual (atopic) leading to tissue damage.
Why hypersensitivity occurs in some people? (not all)  Allergins  Low immunity from childhood  Host factors include heredity, gender, race, and age, with heredity being by far the most significant.  However, there have been recent increases in the incidence of allergic disorders that cannot be explained by genetic factors alone.  Four major environmental candidates are alterations in exposure to infectious diseases during early childhood, environmental pollution, allergen levels, and dietary changes.
Types of Hypersensitivity: Nearly 45 years ago Gell and Coombs proposed a classification scheme which defined 4 types of Hypersensitivity type I hypersensitivity reactions. Ab mediated: type:Ⅰ, Ⅱ, Ⅲ Hypersensitivity type II (Immediate) T-cell mediated: type Ⅳ (Delayed) Hypersensitivity type III Hypersensitivity type IV
Hyper sensitivity type I: IgE mediated, immediate hypersensitivity/ allergy Major features: React and disappear quickly on re-exposure to Ag Dysfunction rather than severe tissue and cell damage occurs Obvious individual difference and genetic correlation By mast cells and basophils
MECHANISM OF ACTION BASIC ELEMENTS ARE: 1. MEDIATOR = IgE 2. PRIMARY CELLULAR COMPONENT = MAST CELL AND BASOPHILS 3. AMPLIFIER = PLATELETS, NEUTROPHILS AND EIOSINOPHILS
MECHANISM OF ACTION
MECHANISM OF ACTION STEP 1: EXPOSURE OF ANTIGEN TO ANTIGEN PRESENTING CELL
MECHANISM OF ACTION STEP 2: RECOGNITION BY T- HELPER CELLS ACTIVATION OF B-CELLS INTO PLASMA AND MEMORY CELLS SECRETION OF ANTIBODIES (IgE)
MECHANISM OF ACTION STEP 3: IgE BINDS TO HIGH AFFINITY RECEPTORS (FC EPSILONRI) ON THE SURFACE OF MAST CELLS
MECHANISM OF ACTION STEP 4: SUBSEQUENT EXPOSURE OF ANTIGEN ANTIGEN BINDS WITH IgE ON THE SURFACE OF MAST CELLS
Mechanism of action
MECHANISM OF ACTION STEP 5: RELEASE OF PRIMARY INFLAMMATORY METABOLTES ACTIVATION OF SECONDARY METABOLITES
SYMPTOMS 1. May vary from minor inconvenience to death 2. Usually take 10 to 30 mins to appear after exposure to antigen 3. Sometimes delayed onset of reaction (10- 12h)
MECHANISM OF ACTION MOLECULE EFFECTS PRIMARY MEDIATORS HISTAMINE VASCULAR PERMEABILITY, SMOOTH MUSCLE CONTRACTION SEROTONIN VASCULAR PERMEABILITY, SMOOTH MUSCLE CONTRACTION ECF-A EOSINOPHIL CHEMOTAXIS NCF-A NEUTROPHIL CHEMOTAXIS PROTEASES MUCUS SECRETION, CONNECTIVE TISSUE DEGRADATION SECONDARY MEDIATORS LEUKOTRIENES VASCULAR PERMEABILITY, SMOOTH MUSCLE CONTRACTION PROSTAGLANDINS VASCULAR PERMEABILITY, SMOOTH MUSCLE CONTRACTION AND PLATELET ACTIVATION BRADYKININ VASCULAR PERMEABILITY, SMOOTH MUSCLE CONTRACTION CYTOKINES NUMEROUS EFFECTS INC. ACTIVATION OF VASCULAR ENDOTHELIUM, EOSINOPHIL RECRUITMENT AND ACTIVATION
CLINICAL"a serious allergic reaction that is rapid Anaphylaxis is defined as DISEASES in onset and may cause death". It typically results in a number of symptoms including an itchy rash, throat swelling, and low blood pressure. Common causes include insect bites, foods, and medications. Anaphylaxis Asthma (from the Greek, "panting") is the common chronic inflammatory disease of the airways characterized by variable and recurring symptoms, reversible airflow obstruction, etc Allergic rhinitis is an allergic inflammation of the nasal airways. It Asthma occurs when an allergen, such as pollen, dust or animal dander (particles of shed skin and hair) is inhaled by an individual with a sensitized immune system. The protein in the food is the most common allergic component. These kinds of allergies occur when the body's immune system mistakenly identifies a protein as harmful. Some proteins or Allergic Rhinitis fragments of proteins are resistant to digestion and those that are tagged by the IgE. The immune system, thinking the organism (the individual) is under attack, triggers an allergic reaction. These reactions can range from mild to severe. Allergic responses include dermatitis, gastrointestinal and respiratory distress, including such life-threatening anaphylactic responses and vasodilation; these require immediate emergency intervention. Individuals with protein allergies commonly avoid contact with the problematic protein. Some medications may prevent, minimize or treat protein allergy reactions. injectable form of epinephrine such as an EpiPen
DIAGNOSTIC TESTS 1. PRICK TEST 2. TRANSDERMAL TEST 3. ELISA
TREATMENT 1. ANTIHISTAMINES 2. Chromolyn sodium 3. leukotriene receptor blockers 4. use of IgG antibodies
Hyper sensitivity type II: Definition: A hypersensitivity resulting from antibodies mistakenly reacting with normal self antigens on body cells. Binding of the antibodies to these normal cells results in immune destruction.
MEDIATORS IgG OR IgM IN THIS CASE 1. MADE AGAINST SELF ANTIGENS 2. ATTACH TO THE SURFACES OF CELLS HAVING SELF EPITOPS SELF ANTIGEN=Any constituent of the body's own tissues capable of stimulating autoimmunity
FACTORS FOR RELEASE OF MEDIATORS 1. FAILURE IN IMMUNE TOLERANCE 2. ENTERANCE OF FOREIGN ANTIGEN RESEMBLING SOME MOLECULE ON THE SURFACE OF HOST CELLS  'IMMUNE TOLERANCE' is the process by which the immune system does not attack an antigen
MECHANISM OF ACTION THESE FACTORS LEAD TO: 1. OPSONIZATION 2. MAC LYSIS 3. ADCC
1- OPSONIZATION DEFINITION: The attachment of microbes and other foreign cells to phagocytes by antibody molecules such as IgG and complement proteins such as C3b. Also called enhanced attachment or immune adherence.
OPSONIZATION MECHANISM THE OPSONIZATION IS OF THE HOST CELL PHAGOCYTES STICK TO MEMBRANES OF HOST CELL VIA IgG, C3B, C4B PHAGOCYTES DISCHARGE THEIR LYSOSOMES
OPSONIZATION RESULT: LYSIS OF HOST CELL
2- MAC LYSIS DEFINITION A protein complex produced during the complement pathways. C5b6789 (MAC or membrane attack complex) puts pores into lipid bilayer membranes of human cells to which antibodies have bound. This results in cell lysis.
MAC LYSIS MECHANISM IgG / IgM BINDS WITH EPITOPS ON CELL SURFACES ACTIVATE CLASSICAL PATHWAY OF COMPLEMENT SYSTEM MAC CAUSES LYSIS OF CELL
MAC LYSIS MECHANISM
3-ANTI-BODY DEPENDENT CYTOTOXICITY (ADCC) DEFINITION The process of NK cells binding to the Fc portion of antibodies that have bound to epitopes of cells recognized as nonself such as infected cells and tumor cells. Once bound to the Fc portion of the antibody, the NK cell will then lyse that cell with perforins.
ADCC MECHANISM IgG / IgM BINDS WITH EPITOPS ON CELL SURFACES NK CELLS ATTACH TO THE Fc PORTION OF IgG/IgM RELEASE OF PERFORINS AND GRANZYMES BY NK APOPTOSIS
ADCC MECHANISM
ADCC MECHANISM
EXAMPLES OF TYPE 2 HYPERSENSITIVITY  AB AND RH BLOOD GROUP REACTIONS;  AUTOIMMUNE DISEASES SUCH AS:  RHEUMATIC FEVER where antibodies result in joint and heart valve damage;  IDIOPATHIC THROMBOCYTOPENIA PURPURA where antibodies result in the destruction of platelets;  MYASTHENIA GRAVIS where antibodies bind to the acetylcholine receptors on muscle cells causing faulty enervation of muscles;  GOODPASTURE'S SYNDROME where antibodies lead to destruction of cells in the kidney;
EXAMPLES OF TYPE 2 HYPERSENSITIVITY  SOME DRUG REACTIONS.  TYPE II HYPERSENSITIVITY ALSO PARTICIPATES IN EARLY TRANSPLANT REJECTIONS.
DIAGNOSTIC TESTS 1. DETECTION OF CIRCULATING ANTIBODY AGAINST THE TISSUES INVOLVED 2. THE PRESENCE OF ANTIBODY AND COMPLEMENT IN THE LESION (BIOPSY) BY IMMUNOFLUORESCENT STAINING (PATTERN = LINEAR).
TREATMENT  ANTI-INFLAMMATORY DRUGS  IMMUNOSUPPRESSANT DRUGS
Hyper sensitivity type III: (THE IMMUNE COMPLEX HYPERSENSITIVITY) Definition: A hypersensitivity resulting from large quantities of soluble antigen- antibody complexes passing between endothelial cells of the blood vessels and becoming trapped on the surrounding basement membrane.
COMPOSITION OF IMMUNE COMPLEX 1. SELF OR NON-SELF ANTIGEN 2. ANTIBODIES MOSTLY IgG RARELY IgM  PATHOLGY OCCURS AT THE SITE OF DEPOSITION
CAUSE OF TYPE 3 HYPERSENSITIVITY NORMALLY SOLUBLE ANTIGEN-ANTIBODY COMPLEX FORMATION REMOVED BY MACROPHAGES IN SPLEEN AND LIVER
CAUSE OF TYPE 3 HYPERSENSITIVITY ABNORMALLY INCREASED SOLUBLE ANTIGEN-ANTIBODY COMPLEX FORMATION NOT ALL REMOVED BY MACROPHAGES IN SPLEEN AND LIVER DEPOSITION OF COMPLEXES VIA BLOOD VESSELS
MECHANISM OF ACTION STEP 1 Large quantities of soluble antigen-antibody complexes form in the blood and are not completely removed by macrophages.
MECHANISM OF ACTION STEP 2 These antigen-antibody complexes lodge in the blood vessels between the endothelial cells and the basement membrane.
MECHANISM OF ACTION STEP 3 These antigen-antibody complexes activate the classical complement pathway leading to vasodilation
MECHANISM OF ACTION STEP 4 The complement proteins and antigen- antibody complexes attract leukocytes to the area.
MECHANISM OF ACTION STEP 5 The leukocytes discharge their killing agents and promote massive inflammation. This can lead to tissue death and hemorrhage.
EXAMPLES OF TYPE 3 HYPERSENSITIVITY 1. SERUM SICKNESS, A COMBINATION TYPE I AND TYPE III HYPERSENSITIVITY 2. AUTOIMMUNE ACUTE GLOMERULONEPHRITIS 3. RHEUMATOID ARTHRITIS 4. SOME CASES OF CHRONIC VIRAL HEPATITIS
DIAGNOSTIC TESTS 1. Examination of tissue biopsies for deposits of immunoglobulins and complement by immunofluorescence (pattern = granular) 2. The presence of immune complexes in serum 3. Depletion in the level of complement
TRAETMENT  ANTI-INFLAMMATORY DRUGS
Hyper sensitivity type IV: (THE CELL MEDIATED OR DELAYEDTYPE HYPERSENSITIVITY) Definition: A hypersensitivity resulting from cell-mediated immunity (cytotoxic T-lymphocytes and cytokines) causing harm to the body.
CAUSE OF TYPE 4 HYPER- SENSITIVITY  CAUSED BY T-CELLS 1. T-HELPER CELLS BY SECRETION OF CYTOKINES 2. MAINLY BY CYTOTOXIC T-CELLS BY DIRECT DAMAGE
MECHANISM OF ACTION T-H CELLS INDUCED STEP 1 ANTIGEN ENTERS THE BODY ENGULFED BY MACROPHAGES PRESENTED TO T-H CELLS T-H CELLS BECOMES ACTIVATED AND INCREASED IN NUMBER
MECHANISM OF ACTION T-H CELLS INDUCED STEP 2 SECOND EXPOSURE ENGULFED BY MACROPHAGES PRESENTED TO T-H CELLS T-H CELLS RELEASE CYTOKINES
MECHANISM OF ACTION T-H CELLS INDUCED STEP 3 T-H 2 CELLS RELEASE T-H 1 or TD CELLS IL-4 AND IL-5 RELEASE CYTOKINES ATTRACTION FOR MORE PROMOTE MACROPHAGES AT THE EXTRACELLULAR SITE OF ATTACK KILLING BY EOSINOPHILS MORE INFLAMMATION TISSUE DAMAGE SKIN LESIONS
MECHANISM OF ACTION CTOTOXICT CELLS INDUCED STEP 1 ANTIGEN BINDS TO NORMAL CELL EPITOPE PRESENTED WITH MHC-1 CTL ATTACHED BY TCR/CD8+ ACTIVATION OF T-CELL
MECHANISM OF ACTION CTOTOXICT CELLS INDUCED STEP 2 ACTIVATION OF CYTOTOXIC T-CELL RELEASE OF 1. PORE-FORMING PROTEINS CALLED PERFORINS 2. PROTEOLYTIC ENZYMES CALLED GRANZYMES 3. CHEMOKINES
MECHANISM OF ACTION CTOTOXICT CELLS INDUCED STEP 3 PERFORINS FORM PORES GRANZYMES PASS THROUGH PORES ACTIVATE ENZYMES OF CELLS APOPTOSIS
MECHANISM OF ACTION CTOTOXICT CELLS INDUCED
EXAMPLES OF TYPE 4 HYPERSENSITIVITY  THE CELL OR TISSUE DAMAGE done during diseases like tuberculosis, leprosy, smallpox, measles, herpes infections.  THE SKIN TEST REACTIONS seen for tuberculosis and other infections  CONTACT DERMATITIS like poison ivy  TYPE -1 INSULIN-DEPENDENT DIABETES where CTLs destroy insulin-producing cells
DIAGNOSTIC TESTS 1. IN VIVO 1. Mantoux test 2. Patch test 2. INVITRO 1. Lympho-cytotoxicity 2. IL-2 production
Allergy