HS type 3 and 4

1. Hypersensitivity Reactions
Dr Anantha Chaitanya J
Intern
BGS GIMS
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2. Hypersensitivity Reaction III
 Immune Complex Mediated.
 Formation of immune complexes in circulation → deposit in various tissues →
trigger classical pathway of complement activation.
 Produce damage as they localize within blood vessel walls or when trapped in
filtering structures (e.g. renal glomeruli)
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3. Hypersensitivity Reaction III3

4. Hypersensitivity Reaction III4

5. Hypersensitivity Reaction III
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ANTIGEN CLINICAL MANIFESTATION
A] EXOGENOUS:
Arthritis
GN, Infective endocarditis
Glomerulonephritis
1) BACTERIA:
Y. enterocolitica
Streptococci
T. pallidum
2) Viruses:
Hepatitis B, CMV Polyarteritis nodosa
3) Parasites:
Plasmodium
Schistosoma
Glomerulonephritis
4) Fungi:
Actinomycetes Farmer’s lung
B] ENDOGENOUS:
SLE1) Nuclear Antigens
2) Immunoglobulins Rheumatoid Arthritis
3) Tumor Antigens Glomerulonephritis

6. Hypersensitivity Reaction III
1. 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,
Arthralgia, Eosinophilia, Splenomegaly, and Lymphadenopathy.
2. ARTHUS REACTION:
 It is named after Dr. Arthus.
 Inflammation caused by the deposition of immune complexes at a localized site.
 Clinical Manifestation is : Hypersensitivity Pneumonitis.
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7. Hypersensitivity Reaction IV
 Cell-mediated hypersensitivity.
 Initiated by sensitized T lymphocytes.
 Principal pattern of immunologic response to intracellular microbiologic agents
(particularly Mycobacterium tuberculosis) as well as viruses, fungi, protozoa &
parasites.
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8. Hypersensitivity Reaction IV
1. Delayed-type hypersensitivity:
 Mediated by CD4 T cells.
 1st exposure to Ag → CD4 T cells + class II MHC → differentiation of naïve CD4 T cells to TH1
cells → release of IL-12, IFN-γ, IL-2, TNFα & lymphotoxin.
 Tuberculin skin test, contact dermatitis, granulomatous inflammation.
2. T Cell-Mediated Cytotoxicity:
 Mediated by CD8+ T cells.
 Sensitized CD8+ T cells kill antigen-bearing target cells.
 Perforin-granzyme-dependent killing → cause perforation of plasma membrane.
 Fas-FasL-dependent killing → activation of apoptosis.
 Graft rejection, virus infections, tumor immunity.
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9. Hypersensitivity Reaction IV9

10. Treatment
 Symptomatic treatment: Anti-histamines, corticosteroids, vasoconstrictors,
smooth muscle relaxants.
 Exposure prevention: Ideal. Not Practical.
 Barriers: Clothes, creams, filters.
 Specific hyposensitization: Test → Identify → Controlled Exposure.
 Nonspecific desensitization: Obsolete.
 Immunoregulation.
 Molecular medicine.
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11. Bibliography
Textbook of Microbiology, Ananthnarayan, 9th
Edition.
IADVL Textbook Of Dermatology, 4th Edition.
Pathologic Basis Of Disease, Robbins and Cotran, 9th
Edition.
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12. Thank You
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