Downloaded 87 times
Uploaded byAnup Bajracharya
Type III Hypersensitivity
Type III hypersensitivity, also known as immune complex-mediated hypersensitivity, occurs when antigen-antibody complexes precipitate in tissues, leading to inflammation and tissue damage via complement activation and cell recruitment. It is primarily mediated by IgG and IgM antibodies against soluble antigens and can result in various conditions such as systemic lupus erythematosus, rheumatoid arthritis, and post-streptococcal glomerulonephritis. The two main forms are localized reactions (arthus reaction) and generalized reactions (serum sickness), characterized by different immune complex responses and resulting symptoms.
More Related Content
Similar to Type III Hypersensitivity
Type III Hypersensitivity
- 1. Type III Hypersensitivity AnupMuni Bajracharya
- 2. ➢ mediated bythe formation of antigen-antibody aggregates called "immune complexes." ➢ also known as immune complex mediated hypersensitivity (antigen-antibody complex mediated destruction of cells). ➢ immune complexes precipitate in various tissues such as skin, joints, vessels, or glomeruli, and trigger the complement pathway. ➢ Complement activation leads to the recruitment of inflammatory cells (monocytes and neutrophils) that release lysosomal enzymes and free radicals at the site of immune complexes, causing tissue damage. ➢ Type III hypersensitivity is primarily mediated by antibodies of the IgG and IgM classes which combine with soluble antigen that are not bound to cell surfaces. The antigens may be self or foreign (i.e., microbial). Type III Hypersensitivity A.B
- 3. . ➢ It involvessoluble antigens that are not bound to cell surfaces (as opposed to those in type II hypersensitivity). ➢ When these antigens bind antibodies, immune complexes of different sizes form. ➢ Large complexes can be cleared by macrophages but macrophages have difficulty in the disposal of small immune complexes. ➢ These immune complexes insert themselves into small blood vessels, joints, and glomeruli, causing symptoms. Like arthiritis, nephritis and vasculitis respectively while less commonly on other organs leading to organ dysfunction. ➢ Wherever immune complexes are deposited, they activate the complement system, and macrophage and neutrophils are attracted to the site, where they cause inflammation leading to tissue injury. Mechanism of Type III (Immune Complex) Hypersensitivity A.B
- 4. Mechanism of TypeIII (Immune Complex) Hypersensitivity A.B
- 5. ➢ Type IIIhypersensitivity reaction develops when immune complex activates C3a and C5a components of complement system. ➢ C3a and C5a are lymphotoxin (anaphylotoxin) that causes localized mast cell degranulation. ➢ Degranulation of mast cell releases histamine which increases vascular permeability of blood capillaries. This facilitates deposition of immune complexes on wall of blood vessel. ➢ C5a, C3a and C5b67 also acts as chemotatic factors for neutrophils, So it attracts neutrophils at the site of immune complex deposition. ➢ C3b acts as opsonin by binding with immune complex. Neutrophil binds to C3b coated immune complex. ➢ The neutrophils attempt to phagocytose the immune complex but phagocytosis is not possible because immune complexes are deposited on basement membrane, so the neutrophil releases lytic enzymes to destroy immune complex. ➢ The lytic enzymes cause tissue damage surrounding of immune complex deposits, resulting hypersensitivity reaction. Furthermore complement proteins can also contribute to tissue destruction. Mechanism of Type III (Immune Complex) Hypersensitivity A.B
- 6. Mechanism of TypeIII (Immune Complex) Hypersensitivity A.B
- 7. Disease Target antigenMain effects Systemic lupus erythematosus Nuclear antigens •Nephritis •Skin lesions •Arthritis Rheumatoid Arthritis Antibody complexes: specifically IgM to IgG •Arthritis Post-streptococcal glomerulonephritis Streptococcal cell wall antigens •Nephritis Serum sickness Various •Arthritis •Vasculitis •Nephritis Arthus reaction Various •Cutaneous vasculitis Farmer's Lung Inhaled antigens (often mould or hay dust) •Alveolar inflammation The most common diseases involving a type III hypersensitivity reaction are A.B
- 8. Forms of TypeIII (Immune Complex) Hypersensitivity • Basically, there are two major forms of immune complex-mediated hypersensitivity • 1. Localized Type III hypersensitivity reaction Arthus reaction • 2. Generalized Type III hypersensitivity reaction Serum sickness A.B
- 9. Arthus reaction Acute Arthusreaction is an example of localized Type III hypersensitivity reaction. The Arthus reaction was discovered by Nicolas Maurice Arthus in 1903. When antigen is injected or enters intradermally or subcutaneously, they bind with antibody to form localized immune complexes which mediate acute Arthus reaction within 4 to 8 hours. As the reaction develops, localized tissue damage and vascular damage results in accumulation of fluids (edema) and RBCs (erythema) at the site of antigen entry. Arthus repeatedly Injected horse serum subcutaneo usly into rabbits. After four injections, he found that there was edema and that the serum was absorbed slowly. Further injections eventually led to gangrene (tissue death caused by a lack of blood supply) A.B
- 10. If an antigenis injected subcutaneously into an animal that already has a very high level of antibodies in its bloodstream, acute inflammation will develop at the injection site within several hours. This is called an Arthus reaction after the scientist who first described it. Antigen injection -→ neutrophil adherence to vascular endothelium By 6 to 8 hours→ the injection site is densely infiltrated by large numbers of these cells. Destruction of blood vessel walls results in hemorrhage and edema, platelet aggregation, and thrombosis. Arthus reaction histological section of an Arthus reaction in the skin of a cat 6 hours after intradermal inoculation of chicken red blood cells. A.B
- 11. Figure: Some ofthe mechanisms involved in the pathogenesis of the Arthus reaction. A.B
- 12. Hypersensitivity Pneumonitis If cattleare fed moldy hay for long periods, constant inhalation of S. rectivirgula spores will result in sensitization and in the development of high- titered antibodies to S. rectivirgula antigens in serum. Eventually inhaled spore antigens will encounter antibodies within the alveolar walls, and the resulting immune complexes and complement activation will cause a pneumonia (or pneumonitis), the basis of which is a type III hypersensitivity reaction. A.B
- 13. Type Specific antigenExposure Bird fancier's lung Also called bird breeder's lung, pigeon breeder's lung, and poultry worker's lung Avian proteins Feathers and bird droppings Bagassosis Exposure to moldy molasses Thermophilic actinomycetes Moldy bagasse (pressed sugarcane) Farmer's lung •The molds Aspergillus species The bacteria •Thermophilic actinomycetes •Thermoactinomyces vulgaris •Saccharopolyspora rectivirgula •Absidia corymbifera •Eurotium amstelodami Moldy hay Cheese-washer's lung Penicillum casei or P. roqueforti Cheese casings Coffee worker's lung Coffee bean protein Coffee bean dust Compost lung Aspergillus Compost Detergent worker's disease Bacillus subtilis enzymes Detergent Hypersensitivity pneumonitis may also be called many different names, based on the provoking antigen These include: A.B
- 14. Systemic Immune ComplexDisease • Serum sickness is an example of generalized Type III hypersensitivity reaction. • When large amount of antigen enter blood stream and bind to antibody, circulating immune complexes forms. • If antigens are in significantly excess compared to antibody, the immune complexes formed are smaller and soluble which are not phagocytized by phagocytic cells leading to Type III hypersensitivity reaction. • The manifestation of serum sickness depends on the quantity of immune complex as well as overall site of deposition. The site may vary but accumulation of complexes occurs at site of blood filtration. • Generalized Type III hypersensitivity reaction at different site results in different diseases such as Glomerulonephritis (Kideny), vasculitis (arteries), Arthritis (synovial joints). A.B
- 15.
- 16. Systemic Lupus Erythematosus(SLE) A.B
- 17.
- 18.
- 19.