HYPERSENSITIVITY REACTIONS TYPE III&IV

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HYPERSENSITIVITY REACTIONS TYPE III&IV LEARNING OBJECTIVES By the end of the lecture student should be able to understand: What is type III Hypersensitivity reactions Different eg type III of

1 HYPERSENSITIVITY REACTIONS TYPE III&IV LEARNING OBJECTIVES By the end of the lecture student should be able to understand: What is type III Hypersensitivity reactions Different eg type III of hypersensitivity reactions What is type IV hypersensitivity reactions Different eg of type IV hypersensitivity reactions. Hypersensitivity It is a process of reactions of antigen with antibody (or) sensitized lymphocytes that are harmful to the host When an adaptive immune response occur in an exaggerated or inappropriate form causing tissue damage, the term hypersensitivity is applied Gell & Coombs classification There are four types of hypersensitivity reactions It is characterized by an allergic reaction immediately following contact with the antigen, which is referred to as the Allergen Type III Hypersensitivity or Immune Complex H.S. Immune complex hypersensitivity occur when antigen-antibody complexes induce an inflammatory response in tissues Normally immune complexes are removed by the reticuloendothelial system, but occasionally they persist and deposited in tissues, resulting in several disorders Deposition of immune complexes activate complement system PMN cells are attracted to the site, hence inflammation and tissue injury take place. Two typical type III Hypersensitivity reactions.

2 1. Arthus Reaction There is inflammation caused by the deposition of immune complexes at a localized site in and found the walls of small blood vessels However most frequently it is demonstrated in the skin On injecting antigen S/C a reaction develops which reaches peak intensity in 4 to 10 hours Arthus Reaction There is marked edema and haemorrhage at the site of injection There reaction finally decreased after 48 hours Infected antigen combines with specific antibody to form immune complexes These complexes activate complement system followed by PMN infiltration and act on platelets, releasing vasoactive amines Arthus Reaction There is intravascular clumping of platelets leads to vascular occulusion and necrosis After 24 to 48 hours these PMN replaced by mononuclear cells and plasma cells appears.

3 2. Serum Sickness It is a systemic inflammatory response to the presence of immune complexes deposited in many area of the body After the injection of foreign serum the production of antibody starts, leads to the formation of immune complexes These immune complexes they may circulate or deposited at various sites In typical S sickness there is fever, utricaria, arthralgia, lymphadenopathy, splenomegally and eosionphilia a few days to 2 weeks after injection Immune Complex Diseases 1. Mysthenia gravis: (antibodies to receptors) Antibodies to Acetylcholine receptors of Neuromuscular junction cause Severe muscular weakness 2. Systemic lupus erythematosus (SLE) Auto-antibodies against DNA, histones, nucleolar proteins and other components of cell nucleus Inducing agent Not known (most cases) Auto-antibodies are formed 3. Rheumatoid arthritis (RA)

4 against IgG These auto-antibodies are called as rheumatoid factors and are of IgM class People with HLA-DR4 genes are predisposing to RA Trigger agent not known Immune complexes activate complement tissue damage 4. Goodpasture s syndrome: Auto-antibodies are formed against the collagen in basement membranes of the kidney and lungs The agent that induces these auto-antibodies are known but disease occur after a viral infection Pathogenesis: Auto-antibodies Activate compliment system Damage the tissues of Kidney and lung Clinical findings appear. TYPE IV: OR CELL MEDIATED HYPERSENSITIVITY Delayed hypersensitivity is a function of T-lymphocytes, not antibody, causing harm to body The response is delayed i.e. it starts hours or days after contact with the antigen often last for days Clinically important delayed hypersensitivity reactions 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 T- H CELLS INDUCED

5 STEP 2 SECOND EXPOSURE ENGULFED BY MACROPHAGES PRESENTED TO T- H CELLS T- H CELLS RELEASE CYTOKINES STEP 3 T- H CELLS INDUCED T- H 1 or T D CELLS RELEASE CYTOKINES ATTRACTION FOR MORE MACROPHAGES AT THE SITE OF ATTACK MORE INFLAMMATION SKIN LESIONS T- H 2 CELLS RELEASE IL-4 AND IL-5 PROMOTE EXTRACELLULAR KILLING BY EOSINOPHILS TISSUE DAMAGE

6 STEP 1 CTOTOXIC T CELLS INDUCED ANTIGEN BINDS TO NORMAL CELL EPITOPE PRESENTED WITH MHC-1 CTL ATTACHED BY TCR/CD8+ STEP 2 ACTIVATION OF T-CELL CTOTOXIC T CELLS INDUCED ACTIVATION OF CYTOTOXIC T-CELL RELEASE OF o PORE-FORMING PROTEINS CALLED PERFORINS PROTEOLYTIC ENZYMES CALLED GRANZYMES CHEMOKINES

7 STEP 3 CTOTOXIC T CELLS INDUCED PERFORINS FORM PORES GRANZYMES PASS THROUGH PORES ACTIVATE ENZYMES OF CELLS APOPTOSIS CTOTOXIC T CELLS INDUCED a) Contact Hypersensitivity It occurs after sensitization with simple chemicals like nicke and formaldehyde, plant materials, topically applied drugs like sulphonamide, nedmycin, some cosmetics, soaps, etc. In all these cases their small molecules enters the skin, attach to body protein and become complete antigen The immune system recognized it as foreign, cell mediated hypersensitivity is induced, particularly in skin

8 Contact Hypersensitivity Upon a later skin contact with the offending agent, the sensitized person developes erythema, itching, vesicles, eczema or necrosis of skin with in hours Patch skin test on small area of skin can sometimes identify the offending antigen Subsequent avoiding of material will prevent recurrence b) Tuberculin Type Hypersensitivity A small amount of tuberculin (PPD) given intradermally to a previously exposed persons to M.Tuberculosis In duration and redness develops and reached at peak in 48 to 72 hours A positive skin test indicates that a person has been infected with the agent Tuberculin Type Hypersensitivity A positive skin test response assist in diagnosis and provides support for treatment. For example in leprosy, a positive lepromin test indicates the presence of tuberculoid leprosy with competent cell mediated immunity on the other hand if lepromin test is negative suggest the presence of lepromatous leprosy with impaired cell mediate immunity Refrence:pathology basis of diseases robbins 8 th edition pages XXXXXXXXXXXXXXXXXXXThank YouXXXXXXXXXXXXXXXXX

ANIMALS FORM & FUNCTION BODY DEFENSES NONSPECIFIC DEFENSES PHYSICAL BARRIERS PHAGOCYTES. Animals Form & Function Activity #4 page 1

ANIMALS FORM & FUNCTION BODY DEFENSES NONSPECIFIC DEFENSES PHYSICAL BARRIERS PHAGOCYTES. Animals Form & Function Activity #4 page 1 AP BIOLOGY ANIMALS FORM & FUNCTION ACTIVITY #4 NAME DATE HOUR BODY DEFENSES NONSPECIFIC DEFENSES PHYSICAL BARRIERS PHAGOCYTES Animals Form & Function Activity #4 page 1 INFLAMMATORY RESPONSE ANTIMICROBIAL