Type III Hypersensitivity Reaction Quiz

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Questions and Answers

What is the primary component of a granuloma seen in granulomatous inflammation?

Perforin

Fas ligand

Epithelioid cells (correct)

Cytotoxic T lymphocytes

What is the primary consequence of the deposition of antigen-antibody complexes in the renal glomeruli?

Formation of kidney stones

Decreased urine output without complications

Increased blood flow to the kidneys

Vasculitis and endothelial damage (correct)

Which process is primarily mediated by CD4+ T cells in response to a purified protein derivative injection?

Acute inflammatory response

Delayed-type hypersensitivity (correct)

Cytotoxic killing

Immediate hypersensitivity

In which phase of serum sickness does the formation of immune complexes occur?

Before the inflammatory reaction Signup and view all the answers

What characterizes the tuberculin reaction at the injection site after 24 to 72 hours?

Induration peaking at 1 to 2 cm Signup and view all the answers

Which clinical feature is most commonly associated with serum sickness?

Fever and chills Signup and view all the answers

What type of hypersensitivity is associated with contact dermatitis?

Type IV hypersensitivity Signup and view all the answers

What characterizes type IV hypersensitivity reactions?

Delays in response of 48 to 72 hours Signup and view all the answers

What type of cells are primarily responsible for the delayed-type hypersensitivity reaction?

T lymphocytes Signup and view all the answers

What is the mechanism involved in CD8+ T cell-mediated direct cell toxicity?

Perforin-granzymes system and Fas ligand Signup and view all the answers

Which of the following is NOT a potential site of deposition for immune complexes in serum sickness?

Nervous system Signup and view all the answers

What defines the characteristic 'cuffing' observed microscopically in tuberculin reactions?

Perivascular accumulation of T cells and macrophages Signup and view all the answers

What pathological formation results from a prolonged delayed-type hypersensitivity reaction?

Granuloma Signup and view all the answers

What type of pathological reaction occurs against organ transplantation?

Type IV hypersensitivity Signup and view all the answers

What is often modified in self-proteins during drug reactions causing hypersensitivity?

MHC molecules Signup and view all the answers

Which of the following might develop 1-2 weeks after a throat infection due to streptococcal antigens?

Acute post-streptococcal glomerulonephritis Signup and view all the answers

What primarily characterizes Type III hypersensitivity reactions?

Deposition of immune complexes in tissues Signup and view all the answers

Which antibodies are typically involved in Type III hypersensitivity reactions?

IgG, IgM, and occasionally IgA Signup and view all the answers

What is a key clinical manifestation of the Arthus reaction?

Localized tissue necrosis and necrosis at the injection site Signup and view all the answers

Which of the following is NOT an example of a systemic Type III hypersensitivity reaction?

Arthus reaction Signup and view all the answers

In systemic lupus erythematosus (SLE), the autoantibodies target which of the following?

Nuclear components such as DNA and histones Signup and view all the answers

Which of the following describes a common experimental method to induce the Arthus reaction?

Intracutaneous injection of an antigen in a previously immunized animal Signup and view all the answers

What type of necrosis is typically observed at the site of immune complex deposition during an Arthus reaction?

Fibrinoid necrosis Signup and view all the answers

Which of the following best describes serum sickness?

Systemic immune response to foreign serum proteins Signup and view all the answers

Study Notes

Type III Hypersensitivity Reaction (Immune Complex HSR)

Characterized by the formation of immune complexes, either locally in tissues or circulating in the blood and depositing in various tissues.
Antibodies involved are complement-fixing, mainly IgG, IgM, and occasionally IgA.
Antigens can be exogenous (e.g., foreign serum proteins like diphtheria antitoxin, horse anti-thymocyte globulin, or microbial proteins) or endogenous, like DNA antigens.

Mechanism of Type III HSR

Immune complexes form when antigens bind to antibodies.
These complexes deposit in various tissues, leading to complement activation and inflammation.
Complement activation attracts inflammatory cells, leading to tissue damage.

Clinical Examples of Localized HSR III

Arthus Reaction:
- A localized area of tissue necrosis, usually in the skin, caused by acute immune complex vasculitis.
- Induced by intracutaneous injection of an antigen into a previously immunized animal, leading to immune complex formation in the vessel walls.
- Characterized by pain, swelling, induration, edema, and potentially necrosis or ulceration.

Clinical Examples of Systemic HSR III

Serum Sickness:
- Previously common following the administration of vaccines from other species (e.g., horse or rabbit serum).
- Now less frequent, but can occur with the administration of antibodies from other individuals or species (e.g., horse antithymocyte globulin).
- Pathogenesis involves three phases:
  - Formation of immune complexes (occurs about a week after injection of the foreign protein).
  - Deposition of immune complexes (in blood vessels, renal glomeruli, and joints).
  - Inflammatory reaction and tissue injury.
- Clinical features include fever, urticaria, joint pain (arthralgias), lymph node enlargement, and proteinuria.
Acute Post-streptococcal Glomerulonephritis:
- Develops one to two weeks after throat infection.
- Streptococcal antigens enter the bloodstream, leading to antibody formation and immune complex deposition in the basement membrane of the glomerular capillaries.
- Clinical presentation includes hematuria and oliguria.
Systemic Lupus Erythematosus (SLE):
- An autoimmune disease resulting from autoantibodies against nuclear components (DNA, histones, etc.).
- These antigens are normally sequestered inside the nucleus, but are released following tissue injury (e.g., viral infection).
- Immune complex deposition in basement membranes of glomeruli, lungs, joints, skin, and lymph nodes leads to complement fixation, inflammation, and tissue damage.
- Clinical features are diverse and can be chronic or acute.

Type IV Hypersensitivity (Delayed-Type Hypersensitivity, DTH)

Characterized by a cell-mediated response, primarily involving T lymphocytes (CD4+ and CD8+).
Reaction is delayed, appearing 48 to 72 hours after exposure to the antigen.
CD4+ T cells are activated by non-degradable agents like bacteria, fungi, and protozoa.

Mechanism of Type IV HSR

Activated T cells release cytokines that attract and activate macrophages.
These macrophages can engulf and destroy antigens.
Prolonged DTH responses to persistent microbes or foreign bodies can form granulomas.

Granuloma Formation

Granulomas are localized collections of epithelioid cells surrounded by lymphocytes.
They are often seen in response to persistent microbes, like Mycobacterium tuberculosis.

Clinical Examples of CD4+ T Cell-Mediated Inflammatory Reactions

Tuberculin Reaction (Mantoux Test):
- A classic example of DTH.
- Produced by intracutaneous injection of purified protein derivative (PPD, tuberculin), a protein antigen of Mycobacterium tuberculosis.
- In a previously sensitized individual, the injection site becomes red and indurated 8 to 12 hours after injection, peaking in 24 to 72 hours.
- Microscopically, there is perivascular accumulation of CD4+ T cells and macrophages.
Contact Dermatitis:
- A common skin condition caused by DTH reactions to environmental chemicals.
- The chemical often binds to skin proteins, modifying them and making them recognized as foreign by T cells.
- Presents with vesicular dermatitis (blister-like rash).
Drug Reactions:
- Many drug reactions are mediated by DTH, often manifesting as skin rashes.
- The drug can alter self-proteins, including MHC molecules, leading to recognition of these neoantigens as foreign by T cells.

Direct Cell Toxicity Mediated by CD8+ T Cells

CD8+ T cells (cytotoxic T lymphocytes, CTLs) directly kill antigen-bearing target cells.
This is important in eliminating virus-infected cells and some tumor cells.

Mechanisms of Cytotoxic T Cell-Mediated Killing

Perforin-granzyme system: CTLs release perforin, which forms pores in the target cell membrane, allowing granzymes (enzymes) to enter and induce apoptosis.
Through Fas ligand: CTLs express Fas ligand, which binds to Fas receptor on target cells, triggering the apoptotic pathway.

Examples of Type IV Reactions

Reactions against mycobacterial infections (e.g., tuberculin reaction, granulomatous reactions in tuberculosis and leprosy).
Reactions against organ transplantation (leading to rejection).

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Description

Test your knowledge on Type III hypersensitivity reactions, including the formation and mechanisms of immune complexes. Explore clinical examples such as the Arthus reaction and understand the role of antibodies and antigens. This quiz will enhance your understanding of this critical aspect of immunology.