Page 117 - Concise Pathology for Exam Preparation ( PDFDrive )

102 SECTION I General Pathology

Q. What is Arthus reaction?

Ans. Arthus reaction (localized immune complex disease) typically manifests as a localized
area of tissue necrosis resulting from acute immune complex vasculitis involving complement
fixing antibodies IgG and IgM.
• �It is usually elicited in the skin.
• �Intracutaneous injection into an animal having circulating antibodies against the antigen
result in formation of large immune complexes, which precipitate locally and trigger an
inflammatory reaction.
• �Oedema, haemorrhage and ulceration develop in a few hours and peak in 4–10 h after
injection.

Clinical Significance

• �Single large exposure of antigen causes resolution of the disease due to catabolism of

immune complexes (eg, acute serum sickness, acute post-streptococcal glomerulo-

nephritis).
• �Prolonged exposure to antigen causes chronic disease (eg, SLE).
Q. Write in detail on type IV hypersensitivity.
Ans. Type IV (delayed) hypersensitivity is initiated by specifically sensitized T cells and
may be of two types:
1.
Classic delayed hypersensitivity (DTH) mediated by CD41 T cells
Direct cell toxicity (cytolysis) mediated by CD81 T cells

2.
Classic Delayed Hypersensitivity (DTH)
f
It the immunologic response variety intracellular microbiologic agents, eg,
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M. tuberculosis, viruses, fungi, protozoa, parasites, well conditions like contact

dermatitis, type 1 diabetes mellitus, multiple sclerosis and graft rejection. The classic

i

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prototype of DTH tuberculin reaction (intracutaneous injection of tuberculin

(protein–liposaccharide component of tuberculous bacillus) in a previously sensitized

individual resulting in reddening and induration, which starts after 8–12 h and peaks

in 24–72 h.

Morphology of DTH
• �Accumulation of mononuclear cells around small veins and venules producing perivas-
cular cuffing
• �Increased microvascular permeability
• �Escape of plasma proteins leading to dermal oedema or deposition of fibrin in intersti-
tium (induration)
• �Fully developed lesions show endothelial hypertrophy and hyperplasia
• �Persistent/nondegradable antigens induce perivascular lymphocytic infiltrate replaced
by macrophages in 2–3 weeks. Macrophages are converted into epithelium-like (epithe-
lioid) cells, which aggregate to for granulomas.
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