Immunopathology — MCQs

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 211: SLE is which type of hypersensitivity reaction?

A. Type I hypersensitivity
B. Type II hypersensitivity
C. Type III hypersensitivity (Correct Answer)
D. Type IV hypersensitivity

Explanation: ### Explanation **Systemic Lupus Erythematosus (SLE)** is primarily classified as a **Type III Hypersensitivity reaction** [1]. **1. Why Type III is Correct:** The hallmark of SLE is the production of **autoantibodies** (e.g., Anti-dsDNA) that bind to self-antigens, forming **circulating immune complexes** [1], [2]. These complexes deposit in various tissues, particularly the renal glomeruli, joints, and small blood vessels [1]. This deposition triggers the **classical complement pathway** (C3, C4 consumption), leading to neutrophil recruitment, inflammation, and subsequent tissue damage (e.g., Lupus Nephritis) [1]. **2. Why other options are incorrect:** * **Type I (Immediate):** Mediated by IgE and mast cell degranulation (e.g., Anaphylaxis, Asthma). SLE does not involve this pathway. * **Type II (Antibody-mediated):** While SLE has Type II components (e.g., autoantibodies directly causing **Autoimmune Hemolytic Anemia** or Thrombocytopenia) [1], the *systemic* manifestations and the disease's core classification are defined by Type III immune complex deposition. * **Type IV (Delayed-type):** Mediated by T-cells (e.g., TB skin test, Contact dermatitis). SLE is primarily an antibody/B-cell driven pathology. **3. High-Yield Clinical Pearls for NEET-PG:** * **Best Screening Test:** ANA (High sensitivity, low specificity) [2]. * **Most Specific Tests:** Anti-dsDNA (correlates with disease activity/nephritis) and Anti-Smith (Sm) antibodies. * **Drug-Induced Lupus:** Associated with **Anti-Histone antibodies** (Common drugs: Hydralazine, Procainamide, Isoniazid). * **Complement Levels:** Characterized by **low C3 and C4** during active flares due to consumption in Type III reactions [1]. * **Libman-Sacks Endocarditis:** Small, sterile, verrucous vegetations on both sides of heart valves. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-216, 230. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 226.

Question 212: Which of the following cytokines are anti-inflammatory in nature?

A. IL-4
B. IL-10
C. TGF-β
D. All of the above (Correct Answer)

Explanation: ### Explanation The correct answer is **D. All of the above**. In immunopathology, cytokines are classified based on their functional role in the inflammatory response. While pro-inflammatory cytokines (like TNF-α, IL-1, and IL-6) drive the immune response, **anti-inflammatory cytokines** serve to limit the intensity of inflammation and promote tissue repair. #### Why the options are correct: * **IL-10:** Often referred to as the "prototypical anti-inflammatory cytokine," it is produced by macrophages and Th2 cells. It inhibits the synthesis of pro-inflammatory cytokines (TNF, IL-12) and downregulates the expression of MHC Class II and co-stimulatory molecules on macrophages, effectively "turning off" the immune response. * **TGF-β (Transforming Growth Factor-beta):** This is a potent immunosuppressive agent. It inhibits the proliferation of T cells and the activation of macrophages. Crucially, it also promotes the synthesis of collagen, shifting the body from an inflammatory phase to a **healing/fibrotic phase**. * **IL-4:** While primarily known for inducing Th2 differentiation and B-cell class switching to IgE, IL-4 also antagonizes the effects of IFN-γ. It promotes the **Alternative Activation of Macrophages (M2 pathway)**, which is involved in tissue repair rather than microbicidal activity [1]. #### NEET-PG High-Yield Pearls: * **M1 vs. M2 Macrophages:** Pro-inflammatory cytokines (IFN-γ) activate the **M1 pathway** (classical), while anti-inflammatory cytokines (IL-4, IL-13) activate the **M2 pathway** (alternative) [1]. * **IL-10 & Cancer:** Some tumors secrete IL-10 to evade the immune system by inhibiting T-cell-mediated anti-tumor responses. * **TGF-β Dual Role:** While anti-inflammatory, chronic overproduction of TGF-β is the primary driver of **organ fibrosis** (e.g., Liver Cirrhosis, Pulmonary Fibrosis). * **IL-1 Receptor Antagonist (IL-1ra):** Another high-yield anti-inflammatory molecule that competitively inhibits IL-1. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 105-106.

Question 213: C-ANCA positivity indicates antibodies formed against which of the following?

A. Proteinase 3 (Correct Answer)
B. Myeloperoxidase
C. Cytoplasmic antinuclear Antibody
D. Anti centromere Antibody

Explanation: **Explanation:** **ANCA (Antineutrophil Cytoplasmic Antibodies)** are autoantibodies directed against enzymes found within the primary granules of neutrophils and lysosomes of monocytes [1]. They are classified based on their immunofluorescence staining patterns: 1. **Why Proteinase 3 (PR3) is correct:** **C-ANCA (Cytoplasmic ANCA)** shows a diffuse granular staining pattern throughout the cytoplasm. The primary target antigen for c-ANCA is **Proteinase 3 (PR3)**. This is highly specific (approx. 95%) for **Granulomatosis with Polyangiitis (GPA)**, formerly known as Wegener’s Granulomatosis. 2. **Why other options are incorrect:** * **Myeloperoxidase (MPO):** This is the target antigen for **p-ANCA (Perinuclear ANCA)**. It is typically associated with Microscopic Polyangiitis (MPA), Churg-Strauss Syndrome (EGPA), and Pauci-immune Crescentic Glomerulonephritis [2]. * **Cytoplasmic Antinuclear Antibody:** This is a misnomer. Antinuclear antibodies (ANA) target antigens within the nucleus, not the cytoplasm, and are markers for systemic autoimmune diseases like SLE [3]. * **Anti-centromere Antibody:** This is a specific marker for **Limited Cutaneous Systemic Sclerosis (CREST Syndrome)**. **High-Yield Clinical Pearls for NEET-PG:** * **GPA (Wegener’s) Triad:** Necrotizing granulomas of the respiratory tract, necrotizing vasculitis, and focal necrotizing glomerulonephritis. * **Monitoring:** C-ANCA titers correlate with disease activity; a rise in titers often precedes a clinical relapse [2]. * **P-ANCA False Positives:** Can occur in Ulcerative Colitis and Primary Sclerosing Cholangitis (atypical p-ANCA). * **Drug-induced ANCA:** Certain drugs like Propylthiouracil and Hydralazine can induce p-ANCA positivity. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 514-515. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 917-918. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 226-227.

Question 214: Thymoma may be associated with all the following conditions, EXCEPT:

A. Polymyositis
B. Sjogren's syndrome
C. Ulcerative colitis
D. Crohn's disease (Correct Answer)

Explanation: **Explanation:** Thymomas are epithelial neoplasms of the thymus that are uniquely associated with a wide spectrum of **paraneoplastic autoimmune syndromes**. This association occurs because the neoplastic thymus fails to properly "educate" T-cells (defective negative selection), leading to the escape of self-reactive T-lymphocytes into the systemic circulation. **Why Crohn’s Disease is the Correct Answer:** While thymomas are linked to various autoimmune conditions, **Crohn’s disease** is notably **not** associated with thymoma. In contrast, **Ulcerative Colitis (Option C)** has a documented, albeit rare, association with thymic tumors. This distinction is a classic "except" style question in pathology exams. **Analysis of Incorrect Options:** * **Polymyositis (Option A):** Inflammatory myopathies (including polymyositis and dermatomyositis) are well-recognized paraneoplastic manifestations of thymoma, second only to Myasthenia Gravis in frequency among muscle-related associations. * **Sjogren’s Syndrome (Option B):** Various connective tissue and rheumatologic diseases, including Sjogren’s syndrome, Systemic Lupus Erythematosus (SLE), and Rheumatoid Arthritis, are associated with thymic epithelial tumors. * **Ulcerative Colitis (Option C):** Inflammatory Bowel Disease, specifically Ulcerative Colitis, is a recognized paraneoplastic association of thymoma, unlike Crohn's disease. **NEET-PG High-Yield Pearls:** 1. **Most Common Association:** **Myasthenia Gravis** (seen in ~30-45% of thymoma patients). 2. **Pure Red Cell Aplasia (PRCA):** A highly specific association; ~50% of PRCA patients have an underlying thymoma. 3. **Hypogammaglobulinemia:** Known as **Good Syndrome** (Thymoma + Hypogammaglobulinemia). 4. **Other Associations:** Graves' disease, Pernicious anemia, and Alopecia areata.

Question 215: Which of the following is NOT a type II hypersensitivity reaction?

A. Hemorrhagic disease of the newborn (Correct Answer)
B. Graves disease
C. Autoimmune hemolytic anemia
D. Acute rheumatic fever

Explanation: **Explanation:** The correct answer is **A. Hemorrhagic disease of the newborn**. **1. Why Hemorrhagic disease of the newborn is NOT Type II Hypersensitivity:** Hemorrhagic disease of the newborn (now commonly called Vitamin K Deficiency Bleeding) is a **coagulation disorder**, not an immunological reaction. It occurs due to a deficiency of Vitamin K-dependent clotting factors (II, VII, IX, and X) because of poor placental transfer and a sterile neonatal gut. *Note:* Do not confuse this with **Hemolytic** Disease of the Newborn (Rh incompatibility), which *is* a classic Type II hypersensitivity reaction involving IgG antibodies against fetal RBCs [2]. **2. Analysis of Incorrect Options (Type II Hypersensitivity Examples):** Type II hypersensitivity involves antibody-mediated (IgG/IgM) destruction or dysfunction of cells [4]. * **Graves’ Disease:** Antibodies (TSI) bind to TSH receptors, simulating thyroid hormone production (Type II non-cytotoxic/stimulatory subtype) [1]. * **Autoimmune Hemolytic Anemia:** Antibodies are directed against self-antigens on Red Blood Cells, leading to their destruction via the complement system or splenic macrophages. * **Acute Rheumatic Fever:** Antibodies produced against Streptococcal M-protein cross-react with myocardial self-antigens (molecular mimicry), causing tissue damage. **3. NEET-PG High-Yield Pearls:** * **Type II Mechanism:** "Cytotoxic" – involves Opsonization, Complement activation, or Antibody-Dependent Cellular Cytotoxicity (ADCC) [3]. * **Mnemonic for Type II:** **"My Blood Group Is A+":** **M**yasthenia gravis, **B**lood transfusion reactions, **G**oodpasture syndrome, **I**nsulin-resistant diabetes (Type B), **S**pecific cell destruction (ITP/AIHA), **A**cute Rheumatic Fever, **P**emphigus vulgaris. * **Distinction:** Graves' and Myasthenia Gravis are specifically "Type II non-cytotoxic" because they alter cell function without necessarily killing the cell [1]. **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] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 627-628. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 214. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210.

Question 216: Which HLA marker is associated with gluten-sensitive enteropathy?

A. DR3 and DQ1
B. DR4
C. B27
D. DQ2 and DQ8 (Correct Answer)

Explanation: **Explanation:** Gluten-sensitive enteropathy (Celiac Disease) is a chronic autoimmune-mediated enteropathy triggered by the ingestion of gluten in genetically predisposed individuals. The pathogenesis involves the deamidation of gliadin peptides by the enzyme tissue transglutaminase (tTG). These negatively charged peptides are then presented by **MHC Class II molecules** to CD4+ T-cells [2]. **Why DQ2 and DQ8 are correct:** The specific HLA alleles **DQ2** (found in ~95% of patients) and **DQ8** have a unique molecular structure that allows them to bind deamidated gliadin peptides with high affinity [1]. This binding is the critical step in initiating the inflammatory cascade that leads to villous atrophy. The absence of these markers has a high negative predictive value (nearly 100%), meaning if a patient lacks both DQ2 and DQ8, Celiac disease is highly unlikely. **Analysis of Incorrect Options:** * **DR3 and DQ1:** While HLA-DR3 is often in linkage disequilibrium with DQ2, DQ1 is not specifically associated with Celiac disease. * **DR4:** This is primarily associated with **Rheumatoid Arthritis** and Type 1 Diabetes Mellitus. * **B27:** This is a Class I HLA marker strongly associated with **Seronegative Spondyloarthropathies** (e.g., Ankylosing Spondylitis, Reiter’s syndrome). **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Small intestinal biopsy showing villous atrophy, crypt hyperplasia, and increased intraepithelial lymphocytes (Marsh Criteria) [2]. * **Serology:** Anti-tissue transglutaminase (tTG) IgA is the screening test of choice. Anti-endomysial antibody (EMA) is highly specific [1]. * **Associated Conditions:** Dermatitis herpetiformis (intense pruritic vesicles), Type 1 Diabetes, and selective IgA deficiency [2]. * **Complication:** Increased risk of Enteropathy-Associated T-cell Lymphoma (EATL). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 360-361. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 789-790.

Question 217: Which defect is identified by the nitroblue tetrazolium test?

A. Phagocytosis (Correct Answer)
B. Complement
C. T cell
D. B cell

Explanation: The **Nitroblue Tetrazolium (NBT) test** is a classic diagnostic tool used to assess the **oxidative burst** capacity of phagocytes (neutrophils and macrophages). Phagocytosis involves the ingestion of pathogens, followed by their destruction via reactive oxygen species (ROS) [1]. This process is mediated by the **NADPH oxidase enzyme complex**. In a normal cell, NADPH oxidase reduces the yellow NBT dye into insoluble, dark blue **formazan crystals**. A positive NBT test (blue color) indicates intact phagocytic killing power. A negative NBT test (no color change) indicates a defect in the oxidative burst, most characteristically seen in **Chronic Granulomatous Disease (CGD)**. Complement defects are typically screened using the **CH50 assay** (for classical pathway) or **AH50** (for alternative pathway). T-cell function is evaluated via delayed-type hypersensitivity (DTH) skin tests, flow cytometry (CD3/CD4/CD8 counts), or mitogen stimulation assays. B-cell function is assessed by measuring serum immunoglobulin levels (IgG, IgA, IgM) or quantifying CD19/CD20+ cells via flow cytometry. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 89-92.

Question 218: Hot agglutinin is found in all conditions except:

A. Mycoplasma infection (Correct Answer)
B. Systemic Lupus Erythematosus (SLE)
C. Methyl dopa
D. Rheumatoid arthritis

Explanation: ### Explanation The question asks to identify the condition associated with **Cold Agglutinins** rather than **Hot (Warm) Agglutinins**. #### 1. The Core Concept: Warm vs. Cold Autoimmune Hemolytic Anemia (AIHA) Autoimmune hemolytic anemia is classified based on the thermal amplitude of the autoantibodies involved: * **Warm Agglutinins (Hot):** These are typically **IgG** antibodies that react optimally at body temperature (**37°C**) [1]. They cause extravascular hemolysis in the spleen [1]. * **Cold Agglutinins:** These are typically **IgM** antibodies that react optimally at low temperatures (**0–4°C**). They cause hemolysis by fixing complement. #### 2. Why "Mycoplasma infection" is the Correct Answer **Mycoplasma pneumoniae** infection is a classic cause of **Cold Agglutinin Disease**. The bacteria express antigens that mimic the **I-antigen** on human red blood cells, leading to the production of cross-reactive IgM antibodies. Therefore, it is NOT associated with Hot (Warm) agglutinins. #### 3. Analysis of Incorrect Options (Causes of Warm/Hot Agglutinins) * **Systemic Lupus Erythematosus (SLE):** This is the most common secondary cause of Warm AIHA (IgG-mediated) [1]. * **Methyl dopa:** A classic drug-induced cause of Warm AIHA [1]. It alters the Rh antigen on RBCs, making them appear foreign to the immune system. * **Rheumatoid arthritis:** Along with other autoimmune connective tissue disorders, RA is frequently associated with Warm (Hot) agglutinins [1]. #### 4. NEET-PG High-Yield Pearls * **Warm AIHA (IgG):** "Warm Weather is Great" (Warm = IgG). Associated with SLE, CLL, and drugs (̑-methyldopa, Penicillin). * **Cold AIHA (IgM):** "Cold Ice Cream" (Cold = IgM). Associated with **Mycoplasma pneumoniae** (anti-I) and **Infectious Mononucleosis/EBV** (anti-i). * **Direct Coombs Test:** Used to diagnose both; it detects antibodies or complement already bound to the patient's RBCs. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603.

Question 219: Which of the following is an organ-specific autoimmune disease?

A. Systemic Lupus Erythematosus (SLE)
B. Rheumatoid Arthritis (RA)
C. Goodpasture's syndrome (Correct Answer)
D. Polyarteritis Nodosa (PAN)

Explanation: Autoimmune diseases are broadly classified into two categories: **Organ-specific** (affecting a single organ or cell type) and **Systemic/Non-organ-specific** (affecting multiple organs and tissues throughout the body) [3]. **Why Goodpasture’s Syndrome is the Correct Answer:** Goodpasture’s syndrome is a classic example of an organ-specific autoimmune disease. It is caused by the formation of **anti-GBM antibodies** directed against the non-collagenous domain of the **α3 chain of Type IV collagen**. This specific antigen is localized primarily in the **glomerular basement membrane (GBM)** of the kidneys and the **alveolar basement membrane** of the lungs [1]. Consequently, the clinical manifestations are restricted to these two sites (Glomerulonephritis and Pulmonary hemorrhage). **Analysis of Incorrect Options:** * **A. Systemic Lupus Erythematosus (SLE):** A prototypical systemic autoimmune disease. It involves a wide array of autoantibodies (like anti-dsDNA) that form immune complexes, causing damage to the skin, joints, kidneys, heart, and serosal membranes [3]. * **B. Rheumatoid Arthritis (RA):** While primarily affecting joints, RA is a systemic inflammatory disorder that can involve the lungs (interstitial fibrosis), skin (nodules), and blood vessels (vasculitis). * **C. Polyarteritis Nodosa (PAN):** A systemic necrotizing vasculitis that affects small and medium-sized muscular arteries throughout the body, leading to multi-organ dysfunction (sparing the lungs). **NEET-PG High-Yield Pearls:** * **Type of Hypersensitivity:** Goodpasture’s syndrome is a **Type II Hypersensitivity** reaction. * **Immunofluorescence (IF):** Characterized by a **Linear** pattern of IgG deposition along the basement membrane (unlike the "lumpy-bumpy" granular pattern seen in Type III reactions like SLE) [1]. * **Other Organ-Specific Examples:** Hashimoto’s thyroiditis, Type 1 Diabetes Mellitus, Myasthenia Gravis, and Graves' disease [2], [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 909. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 213-214. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 219-220.

Question 220: Which of the following cells is NOT involved in HIV infection?

A. Macrophages
B. Lymphocytes
C. Neutrophils (Correct Answer)
D. Dendritic cells

Explanation: The primary target of the Human Immunodeficiency Virus (HIV) is cells expressing the **CD4 receptor** and specific co-receptors (**CCR5** or **CXCR4**) [1]. ### **Why Neutrophils is the Correct Answer** **Neutrophils** do not express CD4 receptors or the necessary chemokine co-receptors on their surface. Therefore, they cannot be directly infected by HIV. While HIV infection leads to quantitative (neutropenia) and qualitative defects in neutrophils due to bone marrow suppression and cytokine imbalances, the virus does not utilize them for entry or replication. ### **Explanation of Incorrect Options** * **Lymphocytes:** Specifically, **CD4+ T-helper cells** are the primary targets [2]. HIV binds to the CD4 molecule via its **gp120** envelope protein, leading to the progressive depletion of these cells, which is the hallmark of AIDS [2]. * **Macrophages:** These cells express CD4 and the **CCR5** co-receptor (M-tropic strains) [2][3]. Macrophages are resistant to the cytopathic effects of HIV; they act as **reservoirs** for the virus and are responsible for transporting it to the Central Nervous System (CNS) [3]. * **Dendritic Cells:** Follicular dendritic cells in lymph nodes and mucosal Langerhans cells trap HIV [3]. They play a critical role in the initial capture of the virus and its presentation/transmission to T-cells in lymphoid tissues. ### **High-Yield NEET-PG Pearls** * **Primary Receptor:** CD4 molecule. * **Co-receptors:** **CCR5** (important for early/mucosal infection; "M-tropic") and **CXCR4** (important for late-stage infection; "T-mropic") [1][2]. * **Genetic Resistance:** Individuals with a homozygous **CCR5-Δ32 mutation** are resistant to HIV infection. * **First cells infected:** Usually intraepithelial dendritic cells or mucosal macrophages. * **Major Reservoir:** Macrophages and Latent Memory T-cells. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 170-171. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 254-255. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 255-258.

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Cells and Tissues of the Immune System

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Innate Immunity

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Adaptive Immunity

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Hypersensitivity Reactions

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Autoimmune Diseases

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Immunodeficiency Disorders

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Transplantation Immunopathology

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Immune Response to Infections

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Immunologic Laboratory Techniques

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Tumor Immunology

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