Immunopathology — MCQs

An 18-year-old man is evaluated for possible immunodeficiency disease due to a lifelong history of chronic lung infections, recurrent otitis media, and multiple episodes of bacterial meningitis. Although total IgG is normal, the patient has a selective deficiency of IgG2. An associated deficiency of which of the following other substances may produce anaphylaxis when blood products are given to such individuals?

Q18Easy

What is the HLA marker associated with Behcet's syndrome?

Q19Easy

Which of the following conditions is associated with ANCA?

Q20Easy

Acute graft rejection typically occurs within what timeframe?

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 11: Acute graft versus host disease reaction occurs in all EXCEPT?

A. Liver
B. Adrenal (Correct Answer)
C. Gut
D. Skin

Explanation: **Explanation:** Acute Graft-Versus-Host Disease (GVHD) occurs when immunocompetent T-cells from a donor graft (the "graft") recognize the recipient’s (the "host") HLA antigens as foreign, leading to an immune-mediated attack [1]. This typically occurs within the first 100 days following hematopoietic stem cell transplantation. **Why Adrenal is the Correct Answer:** Acute GVHD characteristically targets specific epithelial "barrier" organs. The **Adrenal gland is not a target organ** for acute GVHD. The pathophysiology involves a "cytokine storm" and direct T-cell cytotoxicity specifically directed at the skin, gastrointestinal tract, and liver. **Analysis of Other Options:** * **Skin (Option D):** This is the most common and usually the earliest organ affected [1]. It typically presents as a maculopapular rash, often starting on the palms, soles, and neck, which can progress to generalized erythroderma or toxic epidermal necrolysis-like lesions. * **Gut (Option C):** The gastrointestinal tract is a major target. Clinical manifestations include profuse watery diarrhea (often described as "greenish"), abdominal pain, and mucosal ulceration [1]. * **Liver (Option B):** Hepatic involvement is a hallmark of acute GVHD, manifesting as cholestatic jaundice due to the destruction of small bile ducts and rising levels of serum bilirubin and alkaline phosphatase [1]. **NEET-PG High-Yield Pearls:** * **Triad of Acute GVHD:** Dermatitis (Rash), Enteritis (Diarrhea), and Hepatitis (Jaundice). * **Chronic GVHD:** Occurs after 100 days; resembles systemic sclerosis (scleroderma-like skin) and can involve the lungs (bronchiolitis obliterans). * **Prerequisite:** The recipient must be immunocompromised to prevent them from rejecting the donor cells before the donor cells can attack the host. * **Prevention:** Depletion of donor T-cells before transfusion reduces the risk of GVHD but increases the risk of graft failure and recurrence of leukemia (loss of Graft-versus-Leukemia effect). **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. 182-183.

Question 12: Which cell type is primarily involved in immunity against parasitic infections?

A. Neutrophil
B. Eosinophil (Correct Answer)
C. Basophil
D. Lymphocyte

Explanation: **Explanation:** The correct answer is **B. Eosinophil**. **Why Eosinophils are correct:** Eosinophils are specialized granulocytes primarily responsible for combating multicellular parasites (helminths). When a parasite enters the body, it is coated with IgE antibodies (Type I hypersensitivity mechanism). Eosinophils bind to the Fc portion of these IgE antibodies via high-affinity receptors. Once activated, they undergo degranulation, releasing potent cytotoxic proteins such as **Major Basic Protein (MBP)**, Eosinophil Cationic Protein (ECP), and Eosinophil-derived neurotoxin. MBP is specifically toxic to the helminthic wall, leading to the destruction of the parasite. **Why other options are incorrect:** * **Neutrophils:** These are the "first responders" primarily involved in **acute bacterial infections** and sterile inflammation through phagocytosis and NETosis. * **Basophils:** These cells circulate in the blood and are involved in allergic responses and histamine release; while they participate in the Th2 response, they are not the primary effectors against parasites [1]. * **Lymphocytes:** This is a broad category. While B-cells produce the IgE needed and T-cells (Th2) orchestrate the response via IL-5, the "cell type primarily involved" in the direct effector action against the parasite is the eosinophil [1]. **High-Yield Clinical Pearls for NEET-PG:** * **IL-5 Connection:** Interleukin-5 is the most important cytokine for eosinophil recruitment, activation, and survival. * **Charcot-Leyden Crystals:** Found in sputum (asthma) or stool (parasitic infections), these are formed from the breakdown of eosinophil cell membranes (specifically Galectin-10). * **Eosinophilia:** Defined as an absolute eosinophil count >500/µL. Common causes include **NAACP**: **N**eoplasia, **A**sthma/Allergy, **A**ddison’s disease, **C**onnective tissue disorders, and **P**arasites. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 210.

Question 13: Which of the following is NOT true about angioneurotic edema?

A. Pitting edema of face, lips, and mucous membranes (Correct Answer)
B. Can be caused by CI esterase inhibitor deficiency
C. Can be provoked by extreme temperature exposure
D. Is known to be associated with ACE inhibitors

Explanation: **Explanation:** The correct answer is **A**. Angioneurotic edema (angioedema) is characterized by **non-pitting edema**. Unlike the pitting edema seen in congestive heart failure or renal failure (which is caused by fluid accumulation in the interstitium), angioedema involves deep dermal, subcutaneous, or submucosal swelling caused by increased vascular permeability [2]. Because the fluid is often protein-rich or associated with significant tissue tension in deeper layers, it does not leave a persistent indentation upon pressure. **Evaluation of other options:** * **Option B:** Hereditary Angioedema (HAE) is a classic cause, resulting from a deficiency or dysfunction of **C1 esterase inhibitor**. This leads to the over-activation of the complement system and the kinin cascade, resulting in excessive **bradykinin** production [1]. * **Option C:** Physical stimuli, including extreme temperature exposure (cold or heat), trauma, or emotional stress, are well-documented triggers for acute episodes of angioedema in susceptible individuals. * **Option D:** **ACE inhibitors** are a common pharmacological cause of acquired angioedema. They prevent the breakdown of bradykinin (a potent vasodilator), leading to its accumulation and subsequent vascular leakage [1]. **Clinical Pearls for NEET-PG:** * **Key Mediator:** Bradykinin is the primary mediator in HAE and ACE-inhibitor-induced cases; Histamine is the mediator in allergic (Type I Hypersensitivity) cases [1]. * **Life-threatening complication:** Laryngeal edema is the most feared complication, leading to airway obstruction. * **Treatment Hint:** Epinephrine and antihistamines work for allergic types, but HAE requires C1-inhibitor concentrate or Bradykinin-receptor antagonists (e.g., Icatibant). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 100-101. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1164-1166.

Question 14: Hyperacute rejection occurs within:

A. 12 hours (Correct Answer)
B. 2 weeks
C. 1 month
D. 3 months

Explanation: **Explanation:** **Hyperacute rejection** is a Type II hypersensitivity reaction characterized by its rapid onset, occurring within **minutes to a few hours** (typically up to 12–24 hours) after transplantation. It is mediated by **pre-formed antibodies** (IgG) in the recipient's serum against the donor's antigens (usually ABO blood group antigens or HLA Class I antigens). These antibodies bind to the graft endothelium, activating the complement system and leading to immediate thrombosis, fibrinoid necrosis, and graft failure [1]. **Analysis of Options:** * **Option A (12 hours):** This is the correct timeframe. Hyperacute rejection is immediate; if it occurs, it is usually evident before the patient leaves the operating table or within the first few hours post-surgery. * **Option B (2 weeks):** This timeframe is characteristic of **Acute Rejection**, which typically occurs within days to weeks (usually within the first 6 months) [1]. It is primarily T-cell mediated (Type IV hypersensitivity). * **Option C & D (1 month & 3 months):** These timeframes fall under the spectrum of Acute or **Chronic Rejection**. Chronic rejection occurs months to years after transplantation and involves slow, progressive fibrosis and vascular occlusion (e.g., Graft Arteriosclerosis). **High-Yield NEET-PG Pearls:** 1. **Mechanism:** Pre-formed antibodies → Complement activation → Thrombosis [1]. 2. **Gross Appearance:** The graft becomes cyanotic, mottled, and flaccid (often called a "blue kidney") [1]. 3. **Prevention:** It is prevented by **Cross-matching** (testing recipient serum against donor lymphocytes) and ABO typing. 4. **Treatment:** There is no effective treatment once it begins; the graft must be surgically removed [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 241-242.

Question 15: Which antibody is found in myositis?

A. Anti-Jo-1 (Correct Answer)
B. Anti-Scl-70
C. Anti-Sm
D. Anti-Ku

Explanation: **Explanation:** **Inflammatory Myositis** (Polymyositis and Dermatomyositis) is characterized by proximal muscle weakness and elevated muscle enzymes. The diagnosis is supported by specific autoantibodies [1]. **Correct Option: A. Anti-Jo-1** The most common and high-yield "Myositis-Specific Antibody" (MSA) is **Anti-Jo-1**, which is directed against **histidyl-tRNA synthetase** [1]. It is found in approximately 20–30% of patients and is strongly associated with **Antisynthetase Syndrome**, characterized by interstitial lung disease (ILD), "mechanic’s hands," Raynaud's phenomenon, and fever [1]. **Incorrect Options:** * **B. Anti-Scl-70 (Anti-topoisomerase I):** Highly specific for **Diffuse Cutaneous Systemic Sclerosis** [2]. It is associated with a higher risk of pulmonary fibrosis [2]. * **C. Anti-Sm (Anti-Smith):** The most specific antibody for **Systemic Lupus Erythematosus (SLE)** [3]. It is directed against core proteins of small nuclear ribonucleoproteins (snRNPs). * **D. Anti-Ku:** While it can be seen in overlap syndromes involving myositis, it is more classically associated with the overlap of **Systemic Sclerosis and SLE**. **High-Yield Clinical Pearls for NEET-PG:** * **Anti-Mi-2:** Highly specific for **Dermatomyositis**; usually carries a good prognosis and classic skin findings (Gottron papules, Heliotrope rash). * **Anti-SRP (Signal Recognition Particle):** Associated with severe, necrotizing myopathy and poor response to therapy. * **Anti-MDA5:** Associated with clinically amyopathic dermatomyositis and rapidly progressive ILD. * **Screening:** Patients with Dermatomyositis have an increased risk of **visceral malignancies** (lung, ovary, GI tract); age-appropriate cancer screening is mandatory [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1240-1241. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 238-239. [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 16: Plasma cells are activated by which of the following cell types?

A. B cells (Correct Answer)
B. T cells
C. Macrophages
D. Monocytes

Explanation: **Explanation:** The correct answer is **B cells**. This question tests the fundamental understanding of lymphocyte differentiation. Plasma cells are not "activated" by other cells in the traditional sense; rather, they are the **terminally differentiated end-stage** of B cell activation [1]. 1. **Why B cells are correct:** When a B cell encounters an antigen (often with T-cell help), it undergoes clonal expansion and differentiation [3]. A subset of these activated B cells transforms into **plasma cells**, which act as "antibody factories" [1], [2]. Therefore, plasma cells originate directly from B cells. 2. **Why T cells are incorrect:** While Helper T cells (CD4+) are crucial for B cell activation via cytokines (IL-4, IL-5) and CD40-CD40L interaction, they do not directly turn into plasma cells [3]. They facilitate the process, but the precursor cell is the B cell. 3. **Why Macrophages/Monocytes are incorrect:** These are part of the innate immune system and act as Antigen-Presenting Cells (APCs). They process antigens to present them to T cells, initiating the immune cascade, but they do not differentiate into the lymphoid lineage [1]. **High-Yield NEET-PG Pearls:** * **Morphology:** Plasma cells are characterized by an **eccentric nucleus**, "cartwheel" or **"clock-face" chromatin**, and a prominent perinuclear clear zone (Golgi apparatus). * **Russell Bodies:** Eosinophilic cytoplasmic inclusions of packed immunoglobulins found in plasma cells. * **Malignancy:** A neoplastic proliferation of plasma cells leads to **Multiple Myeloma**, characterized by the "M-spike" on electrophoresis. * **Surface Markers:** Unlike B cells, mature plasma cells often lose CD19 and CD20 but express **CD138** (Syndecan-1) and **CD38**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 206-208. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 579-580. [3] 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. 161-162.

Question 17: An 18-year-old man is evaluated for possible immunodeficiency disease due to a lifelong history of chronic lung infections, recurrent otitis media, and multiple episodes of bacterial meningitis. Although total IgG is normal, the patient has a selective deficiency of IgG2. An associated deficiency of which of the following other substances may produce anaphylaxis when blood products are given to such individuals?

A. C3
B. C4
C. IgA (Correct Answer)
D. IgE

Explanation: The patient presents with a history of recurrent sinopulmonary infections and bacterial meningitis, which, combined with a **selective IgG2 deficiency**, is highly suggestive of a primary humoral immunodeficiency. **1. Why IgA is the correct answer:** Selective IgG2 deficiency is frequently associated with **Selective IgA Deficiency**, the most common primary immunodeficiency [2]. Patients with IgA deficiency often develop **anti-IgA antibodies** (IgE type). When these individuals receive blood products (which contain trace amounts of IgA), these pre-formed antibodies trigger a Type I hypersensitivity reaction, leading to life-threatening **anaphylaxis** [1]. This is a classic board-exam association: recurrent infections + IgG subclass deficiency + anaphylaxis during transfusion = IgA deficiency. **2. Why the other options are incorrect:** * **C3 and C4 (Options A & B):** Complement deficiencies (especially C3) lead to recurrent infections with encapsulated bacteria (e.g., *S. pneumoniae*). However, they do not cause anaphylaxis upon blood transfusion. * **IgE (Option D):** IgE is typically elevated in conditions like Job Syndrome (Hyper-IgE syndrome). A deficiency of IgE is rare and does not cause transfusion-related anaphylaxis; rather, IgE is the *mediator* of the anaphylactic reaction in IgA-deficient patients. **Clinical Pearls for NEET-PG:** * **Selective IgA Deficiency:** Defined as serum IgA < 7 mg/dL with normal IgG and IgM. * **Clinical Triad:** Most are asymptomatic, but some present with **S**inopulmonary infections, **A**utoimmune diseases (Celiac, SLE), and **A**topy/Allergy. * **False Positive:** Can cause a false positive pregnancy test (due to heterophile antibodies). * **Management:** If transfusion is necessary, use **washed red blood cells** or blood from an IgA-deficient donor to prevent anaphylaxis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 673-674. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 249-250.

Question 18: What is the HLA marker associated with Behcet's syndrome?

A. HLA-B27
B. HLA-DR5
C. HLA-B51 (Correct Answer)
D. HLA-CW6

Explanation: **Explanation:** **HLA-B51** is the strongest genetic risk factor associated with **Behcet’s Syndrome**, a multi-systemic inflammatory disorder characterized by the triad of recurrent oral ulcers, genital ulcers, and uveitis. While the exact pathogenesis is unknown, it is considered an autoinflammatory vasculitis where HLA-B51 plays a role in neutrophil hyper-reactivity. **Analysis of Options:** * **HLA-B27 (Option A):** This is the classic marker for **Seronegative Spondyloarthropathies**, including Ankylosing Spondylitis (strongest association), Reiter’s syndrome (Reactive arthritis), Psoriatic arthritis, and Enteropathic arthritis [1]. * **HLA-DR5 (Option B):** This marker is primarily associated with **Hashimoto’s thyroiditis** and sometimes Kaposi sarcoma. (Note: HLA-DR3 and DR4 are more commonly tested for autoimmune conditions like SLE and Rheumatoid Arthritis). * **HLA-Cw6 (Option D):** This is strongly linked to **Psoriasis vulgaris**, particularly early-onset (Type I) psoriasis. **High-Yield Clinical Pearls for NEET-PG:** * **Behcet’s Syndrome Triad:** Oral ulcers (most common), Genital ulcers (most specific), and Uveitis. * **Pathergy Test:** A unique diagnostic feature where a minor skin prick leads to the formation of a sterile pustule or papule within 48 hours. * **Geographic Distribution:** Highest prevalence is found along the **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. 49-50.

Question 19: Which of the following conditions is associated with ANCA?

A. Henoch-Schonlein Purpura
B. Wegener’s granulomatosis (Correct Answer)
C. Rheumatoid arthritis
D. Goodpasture syndrome

Explanation: **Explanation:** **Wegener’s Granulomatosis** (now known as Granulomatosis with Polyangiitis - GPA) is the correct answer because it is a classic **ANCA-associated vasculitis** [1]. It is specifically characterized by the presence of **c-ANCA** (cytoplasmic antineutrophil cytoplasmic antibodies), which target the enzyme **Proteinase-3 (PR3)** [1]. Pathologically, it presents as a triad of necrotizing granulomas in the respiratory tract, necrotizing vasculitis of small-to-medium vessels, and renal involvement (pauci-immune glomerulonephritis) [1]. **Analysis of Incorrect Options:** * **Henoch-Schönlein Purpura (HSP):** This is an **IgA-mediated** small vessel vasculitis. It is characterized by IgA immune complex deposition, not ANCA. It typically presents with the tetrad of palpable purpura, arthralgia, abdominal pain, and renal disease. * **Rheumatoid Arthritis:** This is primarily a chronic inflammatory autoimmune disorder characterized by **Rheumatoid Factor (IgM against IgG Fc)** and **Anti-CCP** antibodies. While systemic vasculitis can occur as a complication, it is not primarily an ANCA-associated condition. * **Goodpasture Syndrome:** This is caused by **Anti-GBM antibodies** (Type II hypersensitivity) directed against the alpha-3 chain of Type IV collagen in the glomerular and alveolar basement membranes. It is "pauci-immune" negative, unlike ANCA vasculitides [2]. **NEET-PG High-Yield Pearls:** * **c-ANCA (PR3-ANCA):** Highly specific for Granulomatosis with Polyangiitis (Wegener's) [1]. * **p-ANCA (MPO-ANCA):** Associated with Microscopic Polyangiitis (MPA) and Churg-Strauss Syndrome (Eosinophilic Granulomatosis with Polyangiitis). * **Pauci-immune:** This term refers to the lack of significant antibody or complement deposition on immunofluorescence, a hallmark of ANCA-associated glomerular damage [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 518-520. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 917-918.

Question 20: Acute graft rejection typically occurs within what timeframe?

A. 3 hours
B. 3 days
C. 3 months (Correct Answer)
D. 3 years

Explanation: **Explanation:** The classification of transplant rejection is based on the timing and the underlying immunological mechanism. **Acute rejection** typically occurs within days to a few months (classically within the first **3 months**) post-transplantation [1]. **1. Why "3 months" is correct:** Acute rejection is primarily mediated by **T-cell-mediated immunity** (Type IV hypersensitivity) and/or **humoral immunity** (Type II hypersensitivity) [1]. It involves the activation of recipient T-cells against the donor’s HLA antigens [3]. While it can occur as early as one week, it most frequently manifests within the first 90 days. It is characterized histologically by interstitial mononuclear cell infiltrates and endothelitis [1]. **2. Analysis of Incorrect Options:** * **3 hours (Option A):** This timeframe describes **Hyperacute Rejection**. It occurs within minutes to hours due to pre-formed anti-donor antibodies (e.g., ABO incompatibility), leading to immediate thrombosis and graft necrosis [1]. * **3 days (Option B):** While acute rejection can *start* within days in a sensitized patient (Accelerated Acute Rejection), "3 months" is the standard window used to define the peak period for classic acute rejection episodes [1]. * **3 years (Option D):** This timeframe describes **Chronic Rejection**. It occurs months to years after transplant and is characterized by fibrosis, vascular thickening (arteriosclerosis), and organ atrophy. **High-Yield NEET-PG Pearls:** * **Hyperacute Rejection:** Type II Hypersensitivity; characterized by "Fibrinoid Necrosis" [1]. * **Acute Rejection:** Most common type; manageable with immunosuppressants (e.g., Corticosteroids) [2]. * **Chronic Rejection:** Dominant feature is **intimal fibrosis** and graft arteriosclerosis; generally irreversible. * **GVHD (Graft vs. Host Disease):** Occurs when donor T-cells attack recipient tissues (common in Bone Marrow Transplants). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 241-242. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 242-243. [3] 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. 180-181.

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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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