Immunopathology Practice Questions

Q: The type of allergic reaction seen in allergic fungal sinusitis is -

Type 1 and Type 3. ***Type 1 and Type 3*** - **Allergic fungal sinusitis (AFS)** is primarily characterized by **IgE-mediated hypersensitivity (Type I)** against fungal antigens, manifesting as immediate allergic responses [1]. - **Immune complex formation and deposition (Type III hypersensitivity)** also plays a significant role, contributing to chronic inflammation and tissue damage in the sinuses [2]. - These are considered the **predominant mechanisms** in AFS pathogenesis for clinical and examination purposes. *Type 1 and Type 2* - While **Type I hypersensitivity** (IgE-mediated) is a key component of AFS, **Type II hypersensitivity** (cytotoxic, antibody-dependent) is not involved [1]. - Type II reactions involve antibodies binding to cell surface antigens causing direct cell destruction, which is not a mechanism in AFS [1]. *Type 2 and Type 3* - **Type II hypersensitivity** is not a mechanism in AFS, as the disease does not involve antibody-mediated cellular cytotoxicity [1]. - Although **Type III hypersensitivity** is involved, the absence of Type I (the primary mechanism) makes this option incorrect [2]. *Type 4 and Type 1* - **Type I hypersensitivity** is the primary mechanism in AFS [1]. **Type IV hypersensitivity** (delayed-type, T-cell mediated) may play a contributory role in chronic inflammation. - However, the **classic teaching emphasizes Types I and III** as the predominant hypersensitivity reactions in AFS, with Type I (IgE-mediated) and Type III (immune complex) being the primary drivers of the clinical presentation and pathology [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-211. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215.

Q: Which of the following types of hypersensitivity reactions is primarily involved in Farmer's lung?

Type IV. ***cd*** - Farmer's lung is primarily a **Type III hypersensitivity** reaction [1], which involves the formation of **immune complexes** from inhaled organic antigens, leading to inflammation. - The exposure to moldy hay or organic dust results in **alveolitis**, which characterizes this condition [2]. *ac* - Type I hypersensitivity is **IgE-mediated**, typically causing **immediate allergic reactions**, such as asthma or anaphylaxis. - It does not manifest as chronic lung conditions like Farmer's lung, which has different immunological mechanisms. *ab* - Type II hypersensitivity involves **IgG or IgM antibodies** targeting specific cell surface antigens, leading to cell destruction or dysfunction. - Conditions like hemolytic anemia or autoimmune disorders are examples but are unrelated to Farmer's lung. *bd* - Type IV hypersensitivity is a **cell-mediated response** involving T cells, commonly seen in infections or contact dermatitis. - While it plays a role in certain lung conditions [2], it does not correlate with the immune complex involvement seen in Farmer's lung. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 701-702.

Q: Which type of cells are primarily involved in the infiltration seen in rheumatoid arthritis?

T-cells and B cells. ***T-cells*** - In rheumatoid arthritis, **T-cells** play a crucial role in the **pathogenesis**, contributing to inflammation and joint destruction [1]. - Activated **CD4+ T-cells** are particularly prominent, facilitating the inflammatory processes in the synovium [1]. *NK-cells* - While **Natural Killer (NK) cells** are involved in innate immunity, they are not the predominant infiltrating cells in rheumatoid arthritis. - The condition is primarily driven by **adaptive immune responses**, especially involving T-cells and antibodies. *B cells* - **B cells** contribute to the disease by producing antibodies, but they are not the primary cell type infiltrated [1]. - In rheumatoid arthritis, their role is more about antibody-mediated damage rather than being the dominant infiltrating cells. *Both B & T Cells* - Although both T and B cells are present in rheumatoid arthritis, **T-cells** are the specifically significant infiltrating cells associated with the inflammation. - The focus on **T-cells** highlights the specific adaptive immune response that characterizes this disease [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1212-1214.

Q: Job's syndrome is which of the following types of immunodeficiency disease?

Disorder of phagocytosis. ***Disorder of phagocytosis*** - Job's syndrome (Hyper-IgE syndrome) is primarily classified as a **disorder of phagocytosis** due to defective **neutrophil chemotaxis** - The hallmark feature is **impaired neutrophil migration** to sites of infection, leading to recurrent **staphylococcal skin abscesses** and **pneumonias with pneumatocele formation** - Caused by **STAT3 mutations** (autosomal dominant form), which affect multiple immune pathways but clinically manifest predominantly as phagocyte dysfunction - Classic triad: **elevated IgE** (>2000 IU/mL), **recurrent skin and lung infections**, and **characteristic facies** *Cellular immunodeficiency* - While STAT3 mutations do affect T-cell function (particularly Th17 differentiation), the **primary clinical manifestation** is phagocyte dysfunction - Pure cellular immunodeficiencies like **DiGeorge syndrome** present with viral and fungal infections, which are not the predominant feature in Job's syndrome - The classification is based on the **dominant clinical defect**, which in Job's syndrome is impaired neutrophil chemotaxis *humoral immunodeficiency* - Despite markedly elevated IgE levels, patients have relatively preserved **antibody production** against most pathogens - Humoral deficiencies like **X-linked agammaglobulinemia** present with low immunoglobulin levels and recurrent encapsulated bacterial infections - The elevated IgE in Job's syndrome is a consequence of dysregulated cytokine signaling, not a primary antibody production defect *Disorder of complement* - Complement disorders result from defects in the **complement cascade proteins** (C1-C9) - These typically present with recurrent **Neisseria infections** or autoimmune phenomena like SLE - Job's syndrome does not involve complement pathway defects and presents with characteristic staphylococcal infections

Q: Which antibody is primarily involved in warm antibody autoimmune hemolytic anemia?

IgG. ***IgG*** - **Warm antibody autoimmune hemolytic anemia (wAIHA)** is predominantly mediated by **IgG antibodies** [1]. - These IgG antibodies bind optimally at **37°C (body temperature)**, leading to extravascular hemolysis (primarily in the spleen) [1]. *IgM* - **IgM antibodies** are primarily involved in **cold agglutinin disease**, a type of cold autoimmune hemolytic anemia. - They bind optimally at **lower temperatures (below 37°C)** and often cause intravascular hemolysis. *IgE* - **IgE antibodies** are primarily associated with **allergic reactions** and **parasitic infections**. - They do not play a significant role in the pathophysiology of autoimmune hemolytic anemias. *IgA* - While **IgA antibodies** can occasionally be found in some cases of AIHA, they are generally considered a **minor contributor** and not the primary antibody class in wAIHA. - Their presence often signifies a **mixed-type AIHA** rather than pure warm AIHA. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603.

Q: Which of the following immune hypersensitivity reactions is responsible for Myasthenia Gravis?

Type II Hypersensitivity. ***Type II Hypersensitivity*** - Myasthenia gravis is primarily mediated by **autoantibodies against acetylcholine receptors** [1], characteristic of **Type II hypersensitivity** reactions [3]. - This leads to a reduction in **neuromuscular transmission**, causing muscle weakness and fatigue [1][2]. *Type III Hypersensitivity* - Involves the formation of **immune complexes** that can deposit in tissues, leading to conditions like **lupus** or **glomerulonephritis**. - Myasthenia gravis does not exhibit significant **immune complex** pathology. *Type IV Hypersensitivity* - This is a **delayed-type hypersensitivity reaction**, typically involved in conditions like **tuberculosis** and **contact dermatitis**. - Myasthenia gravis is not primarily mediated by **T-cell** activation which typifies Type IV hypersensitivity. *Type I Hypersensitivity* - Also known as **immediate hypersensitivity** [3], it typically involves **IgE** and reactions like **asthma** and **anaphylaxis**. - Myasthenia gravis does not result from **IgE-mediated** immune responses. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 213-214. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1237-1238. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210.

Q: In a patient with Chronic Granulomatous Disease (CGD) experiencing recurrent bacterial and fungal infections, which specific function of phagocytic leukocytes is primarily impaired due to a defect in the NADPH oxidase system?

Production of reactive oxygen species. ***Production of reactive oxygen species*** - Chronic Granulomatous Disease (CGD) is characterized by a defect in the **NADPH oxidase system**, which is crucial for generating a **respiratory burst**. - This respiratory burst is essential for producing **reactive oxygen species (ROS)** like superoxide radicals, which are vital for killing phagocytosed bacteria and fungi [1]. *Migration to infection sites* - The ability of phagocytes to **migrate to infection sites (chemotaxis)** is generally intact in CGD patients. - Defects in migration are more typically associated with conditions like **Leukocyte Adhesion Deficiency**. *Phagocytosis of pathogens* - Phagocytes in CGD can **engulf pathogens (phagocytosis)** normally [1]. - The defect lies in the **intracellular killing** mechanism *after* phagocytosis, not in the uptake itself [1]. *Presentation of antigens to lymphocytes* - Antigen presentation is a function primarily of **antigen-presenting cells (APCs)** like dendritic cells and macrophages, which is generally unaffected in CGD. - This process is crucial for initiating an **adaptive immune response**, a separate function from the innate pathogen killing defect in CGD. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 91.

Question 1

The type of allergic reaction seen in allergic fungal sinusitis is -

Accepted Answer

Type 1 and Type 3

Answer

Type 2 and Type 3

Answer

Type 1 and Type 2

Answer

Type 4 and Type 1

Question 2

Which of the following types of hypersensitivity reactions is primarily involved in Farmer's lung?

Accepted Answer

Type IV

Answer

Type III

Answer

Type I

Answer

Type II

Question 3

Which type of cells are primarily involved in the infiltration seen in rheumatoid arthritis?

Accepted Answer

T-cells and B cells

Answer

T-cells

Answer

B cells

Answer

NK-cells

Question 4

Job's syndrome is which of the following types of immunodeficiency disease?

Accepted Answer

Disorder of phagocytosis

Answer

humoral immunodeficiency

Answer

Cellular immunodeficiency

Answer

Disorder of complement

Question 5

Which antibody is primarily involved in warm antibody autoimmune hemolytic anemia?

Accepted Answer

IgG

Answer

IgM

Answer

IgE

Answer

IgA

Question 6

Which of the following best denotes classical complement pathway activation in immune inflammatory conditions?

Accepted Answer

C2, C4 and C3 decreased

Answer

C2 and C4 normal, C3 is decreased

Answer

C3 normal and C2, C4 decreased

Answer

C2, C4, C3 all are elevated

Question 7

Which of the following immune hypersensitivity reactions is responsible for Myasthenia Gravis?

Accepted Answer

Type II Hypersensitivity

Answer

Type I Hypersensitivity

Answer

Type III Hypersensitivity

Answer

Type IV Hypersensitivity

Question 8

Cell surface molecules involved in peripheral tolerance induction are

Accepted Answer

B7 and CD28

Answer

CD40 and CD40L

Answer

CD34 and CD51

Answer

B7 and CD3

Question 9

In a patient with Chronic Granulomatous Disease (CGD) experiencing recurrent bacterial and fungal infections, which specific function of phagocytic leukocytes is primarily impaired due to a defect in the NADPH oxidase system?

Accepted Answer

Production of reactive oxygen species

Answer

Migration to infection sites

Answer

Phagocytosis of pathogens

Answer

Presentation of antigens to lymphocytes

Immunopathology — MCQs

Immunopathology — MCQs

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