Notes on Type III Hypersensitivity Reaction
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Notes on Immunology
Notes on Type III Hypersensitivity Reaction
• These reactions are caused when antibody-antigen form complexes and get deposited in tissues. The antibodies mostly being IgG and IgM.
• This is known as Type III hypersensitivity reaction or immune complex disease.
• Ag-Ab union causes acute inflammatory reactions.
• Intensity of reaction depends on amount of Ag and Ab, and relative proportions of reactants.
Examples:
• Arthus reaction (cutaneous) - Time frame for - Onset 1-2 hrs; peak 3-4; disappearance 10-12; symptoms of nonproductive cough, fever, chills, malaise, myalgia, and dyspenia begin 4-6 hr after exposure; symptoms last for 18-48 hrs.
• Serum sickness - injection of heterologous serum or drugs (penicillin); time frame 3 days to 3 weeks; symptoms include fever, splenomegaly, lymphadenopathy, urticarial
• Rash, arthritis, malaise; Clinical examples - allergicpneumontis (Farmer's lung); glomerulonephritis – lumpy-bumpy deposits (SLE, ?-strep, virus) vs smooth deposits (antibody only seen in Goodpasture's disease); rheumatoid arthritis.
Types of Immune Complex diseases:
• Persistent infection + weak Ab response -> chronic immune complex formation -> deposition of complexes in tissues.
• Diseases: Leprosy, Malaria, Dengue, Haemorrhagic fever, Viral hepatitis, Staphylococcal infective endocarditic.
• Autoimmune Disease: immune complex formation -> increased immune complex -> systems responsible for immune complex removal are over worked -> immune complex deposited in tissues.
• Diseases: Rheumatoid Arthritis, Systemic Lupus Erythematosus (SLE), Polymyositis.
• Inhalation of Antigenic material: Extrinsic Ag -> immune complex formed in the body, specifically lungs causing Farmer’s lungs and Pigeon breeder’s lung due to actinomycete fungus infection. This leads to IgG Antibodies and Ag inhalation, causing local immune complex formation in alveoli -> inflammation and fibrosis.
Common immune complex infections:
• Bacterial: Streptococcal, mycoplasma pneumonia, leprosy, and syphilis.
• Viral: Infectious mononucleosis, hepatitis, and dengue hemorrhagic fever.
• Parasitic: malaria, leishmaniasis, trypanosomiasis, and schistosomiasis.
Arthus reaction:
• Ag diffuses in and leads to complex formation.
• Complement activated, C5a and C567. Neutrophils attracted.
• Neutrophils adher to complex and release oxidizing radicals in tissues.
• Blood vessels destroyed, fluid RBCs escape into tissue.
• Anaphylatoxin, kininogen release, platelets, mast cells, local inflammatory responses.
• Platelet aggregation -> microthrombi, vasoactive amines.
• C activation -> polymorph attraction -> proteolytic enzymes, polycations, proteins.
• C activation -> anaphylatoxin -> mast cell mediators.
Hypersensitivity pneumonitis:
• Farmer’s lung, pigeon-breeder’s lung, mushroom grower’s lung.
Multiple antigen exposure: there are two types of reactions:
• Increased size of the basement membrane.
• Deposition on mesangial cells; release of prostaglandins and cytokines; mesangial cell proliferation.
Serum Sickness:
• Acute serum sickness: small soluble complexes pass through basement membrane; there is epithelial cell proliferation.
• Acute serum sickness: larger soluble complexes cannot pass through the basement membrane; there is endothelial cell proliferation.
• Chronic serum sickness: large quantities of complexes deposited peripherally and centrally -> mesangial cell proliferation.
• Chronic serum sickness: small quantities distributed peripherally -> basement membrane thickening.
• Mesangial cell is a modified muscle cell that absorbs immune complexes.
Goodpasture Syndrome:
• Caused by Ab binding to basement membrane of lungs and kidneys.
• Complement system activated.
• Demonstrates “ribbon-like” deposit compared to serum sickness.
Rheumatic fever: Streptococcus infection; common Ag to cardiac muscles, cartilage and glomuler basement membrane.
Glomerulonephritis: Two types of lesions
• Within the glomerulus: complex unable to penetrate basement membrane and deposited under endothelial cells. Smaller complexes penetrate endothelia and basement membrane, and deposited externally. No neutrophils involved.
• Arterial involvement: neutrophil infiltration and destruction of media.
Additional Readings:
Basic Immunology
1. Introduction to Immunology
2. Cells of Immunology
3. Selection of Lymphocytes
4. Primary Response to Antigen
5. Antigen Processing and Presentation
6. Humoral Effector Mechanism Generator
7. Cell-Mediated Effector Mechanism Generator
8. Vaccination and Immunotherapy
9. Immunodeficiency Diseases
10. Acquired Immunodeficiency Syndrome
11. Hypersensitivities and Autoimmunity Diseases
12. Immunology of Transplantation
13. Immunology of Cancer
14. Immunology Laboratory Technology
15. Acquired Immunity
16. Type II Hypersensitivity Reaction
17. Hypersensitivity Reactions
18. Primary Immunodeficiency
19. Secondary Immunodeficiency
20. Type III Hypersensitivity Reaction
21. Type IV Hypersensitivity Reaction
22. Type V Hypersensitivity Reaction
23. Tumor Immunology
24. Images of Antibodies
Related Topics
1. Histology of Lymphoid Tissue
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