Immunopathology — MCQs

Immunopathology Indian Medical PG Practice Questions and MCQs

Question 91: Which cell type lacks HLA antigen?

A. Monocyte
B. Thrombocyte
C. Neutrophil
D. Red blood cell (Correct Answer)

Explanation: The Human Leukocyte Antigen (HLA) system is the human version of the Major Histocompatibility Complex (MHC). **MHC Class I** antigens (HLA-A, B, and C) are expressed on the surface of almost all **nucleated cells** in the body, as well as on platelets. **Why Red Blood Cells (RBCs) are the correct answer:** Mature erythrocytes (RBCs) lack a nucleus and most organelles [1]. Consequently, they **do not express HLA antigens** on their surface. Instead, RBCs express their own specific blood group antigens (ABO and Rh systems). This lack of HLA expression is clinically significant as it prevents HLA-mediated graft-versus-host reactions during simple packed red cell transfusions. **Analysis of Incorrect Options:** * **Monocytes (A) and Neutrophils (C):** As nucleated white blood cells, both are rich in MHC Class I antigens. Monocytes, being professional antigen-presenting cells (APCs), also express **MHC Class II** (HLA-DR, DP, DQ). * **Thrombocytes (B):** Although platelets (thrombocytes) are anucleated fragments of megakaryocytes, they **do express MHC Class I** antigens. This is a high-yield distinction; HLA antibodies can lead to "platelet refractoriness" in multi-transfused patients. **High-Yield Clinical Pearls for NEET-PG:** * **MHC Class I:** Found on all nucleated cells + Platelets (except RBCs). * **MHC Class II:** Found only on Antigen Presenting Cells (Macrophages, B-cells, Dendritic cells) and activated T-cells. * **Exceptions:** Neurons, corneal endothelium, and placental trophoblasts also show very low or absent HLA expression, contributing to their "immune-privileged" status. * **Gene Locus:** HLA genes are located on the **Short arm of Chromosome 6**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 577-586.

Question 92: Which of the following antibody patterns is seen most commonly?

A. IgG (Correct Answer)
B. IgA
C. IgM
D. IgE

Explanation: **Explanation:** In the context of general pathology and immunology, **IgG** is the most common antibody pattern/isotype found in the human body, accounting for approximately **75–80%** of the total serum immunoglobulin pool. **Why IgG is the Correct Answer:** * **Abundance:** It is the most prevalent antibody in the secondary immune response and the only class that crosses the placenta, providing passive immunity to the fetus [1]. * **Half-life:** It has the longest half-life (approx. 23 days), contributing to its high serum concentration. * **Distribution:** It is equally distributed between intravascular and extravascular compartments, making it the dominant antibody seen in most systemic immune reactions and chronic inflammatory patterns. **Why Other Options are Incorrect:** * **IgA:** This is the second most common serum antibody (10–15%) but is the **most abundant in secretions** (tears, saliva, colostrum, and GI tract). * **IgM:** Accounts for about 5–10% of serum antibodies [1]. It is the first antibody produced in a primary immune response and exists as a pentamer [1]. * **IgE:** Found in trace amounts in the serum. It is primarily involved in Type I hypersensitivity reactions and parasitic infections [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Most abundant overall:** IgG. * **Most abundant in secretions:** IgA. * **Largest antibody (Molecular weight):** IgM (Pentamer) [1]. * **Crosses Placenta:** IgG (specifically IgG1, IgG3, and IgG4) [1]. * **Fixes Complement (Classical Pathway):** IgM (most efficient) and IgG [3]. * **Heat Labile Antibody:** IgE (Reaginic antibody). **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. 154-155, 165-166. [2] 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. 171-172. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210.

Question 93: Nitro-blue tetrazolium test is done for which condition?

A. Chronic glomerulonephritis
B. Chronic granulomatous disorder (Correct Answer)
C. Acute granulomatous disease
D. Chediak Higashi syndrome

Explanation: **Explanation:** The **Nitro-blue Tetrazolium (NBT) test** is a classic screening tool used to evaluate the phagocytic function of polymorphonuclear leukocytes (neutrophils). **1. Why Option B is Correct:** **Chronic Granulomatous Disease (CGD)** is caused by a genetic defect in the **NADPH oxidase enzyme** complex. This enzyme is responsible for the "respiratory burst," which produces reactive oxygen species (like superoxide radicals) to kill ingested bacteria. * **The Mechanism:** In the NBT test, colorless NBT dye is added to neutrophils. In healthy cells, NADPH oxidase converts the dye into deep blue-purple **formazan crystals**. * **The Result:** In CGD patients, the lack of NADPH oxidase means the dye remains **colorless/yellow** (Negative NBT test). **2. Why Other Options are Incorrect:** * **A. Chronic Glomerulonephritis:** This is an inflammatory/autoimmune kidney condition diagnosed via urinalysis, renal function tests, and biopsy, not neutrophil function tests. * **C. Acute Granulomatous Disease:** This is a distractor term. CGD is a chronic, hereditary immunodeficiency. * **D. Chediak-Higashi Syndrome:** This is a defect in **lysosomal trafficking (LYST gene)**, characterized by giant cytoplasmic granules [1]. While it affects killing, the primary screening is peripheral blood smear morphology, not the NBT test [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most common form of CGD is **X-linked recessive**. * **Organisms:** Patients are susceptible to **Catalase-positive organisms** (e.g., *S. aureus, Aspergillus, Nocardia, Serratia*) because these bacteria neutralize their own H2O2, leaving the deficient neutrophil with no oxidative tools. * **Modern Gold Standard:** The **Dihydrorhodamine (DHR) flow cytometry test** is now preferred over NBT due to higher sensitivity and quantitative results. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 245-246.

Question 94: Contact dermatitis is an example of which hypersensitivity reaction?

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

Explanation: **Explanation:** **Contact dermatitis** is a classic example of **Type IV (Delayed-type) Hypersensitivity** [1]. This reaction is cell-mediated rather than antibody-mediated. It occurs when a small molecule (hapten), such as nickel or poison ivy, binds to skin proteins [2]. These are processed by Langerhans cells and presented to **CD4+ T-cells (Th1 cells)** [2]. Upon re-exposure, these sensitized T-cells release cytokines (IFN-̳), which activate macrophages and cause keratinocyte damage, leading to the characteristic itchy, vesicular rash [4]. The reaction is "delayed" because it typically takes 24–72 hours to manifest [3]. **Why other options are incorrect:** * **Type I (Immediate):** Mediated by **IgE antibodies** and mast cell degranulation (e.g., Anaphylaxis, Asthma, Urticaria). It occurs within minutes [5]. * **Type II (Cytotoxic):** Mediated by **IgG or IgM** antibodies binding to fixed cell-surface antigens (e.g., Myasthenia gravis, Rheumatic fever, Goodpasture syndrome) [5]. * **Type III (Immune-complex):** Caused by the deposition of **antigen-antibody complexes** in tissues, leading to complement activation (e.g., SLE, Post-streptococcal glomerulonephritis, Arthus reaction) [4]. **Clinical Pearls for NEET-PG:** * **Key Cells:** Type IV hypersensitivity involves **T-lymphocytes** (CD4+ and CD8+), not antibodies [4]. * **Patch Test:** This is the gold standard diagnostic tool for identifying the allergen in contact dermatitis [2]. * **Other Type IV Examples:** Mantoux test (Tuberculin reaction), Graft rejection (acute/chronic), and Granuloma formation (Tuberculosis, Sarcoidosis) [2]. * **Mnemonic:** Remember **ACID** (Type I: **A**naphylactic; Type II: **C**ytotoxic; Type III: **I**mmune-complex; Type IV: **D**elayed). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, p. 1166. [2] 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. 174-175. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 216-218. [4] 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. 173-174. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210.

Question 95: Which interleukin is secreted by Th1 cells?

A. IL-2 (Correct Answer)
B. IL-4
C. IL-10
D. IL-13

Explanation: **Explanation:** The differentiation of Naive T-helper cells (Th0) into specific subsets is a cornerstone of the adaptive immune response. **Th1 cells** are primarily responsible for cell-mediated immunity and the activation of macrophages to destroy intracellular pathogens [1]. **1. Why IL-2 is correct:** Th1 cells are characterized by the secretion of **IL-2**, **IFN-γ (Interferon-gamma)**, and **TNF-β** [3]. * **IL-2** acts as a potent T-cell growth factor, promoting the proliferation of T-cells (autocrine and paracrine) and the differentiation of CD8+ cytotoxic T-cells [4]. * The differentiation of Th1 cells is driven by the transcription factor **T-bet** in response to IL-12 and IFN-γ [1]. **2. Why the other options are incorrect:** * **IL-4 (Option B):** This is the signature cytokine of **Th2 cells** [2]. It promotes B-cell differentiation into plasma cells and induces class switching to **IgE** [2]. * **IL-10 (Option C):** This is an **anti-inflammatory cytokine** produced by Th2 cells and Regulatory T-cells (Tregs). It inhibits Th1 responses by downregulating MHC Class II and IL-12 expression by macrophages. * **IL-13 (Option D):** Produced by **Th2 cells**, it works alongside IL-4 to promote IgE production and mucus secretion in the gut and airways, playing a key role in allergic responses and helminth infections. **High-Yield Clinical Pearls for NEET-PG:** * **Th1 vs. Th2 Balance:** Th1 responses are essential for intracellular organisms (e.g., *Mycobacterium tuberculosis*), while Th2 responses are for extracellular parasites and allergies [1]. * **Leprosy Link:** Tuberculoid leprosy is associated with a strong **Th1 response** (contained infection), whereas Lepromatous leprosy is associated with a **Th2 response** (disseminated infection). * **Transcription Factors:** Th1 = **T-bet**; Th2 = **GATA-3**; Th17 = **RORγt** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 206. [2] 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. [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. 158-160. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 216-218.

Question 96: What percentage of peripheral lymphocytes are null cells?

A. 0-1%
B. 5-10%
C. 10-15% (Correct Answer)
D. 15-20%

Explanation: **Explanation:** In the context of immunopathology, peripheral blood lymphocytes are categorized based on their surface markers and lineage. **Null cells** are a population of lymphocytes that lack the characteristic surface markers of either T-cells (CD3) or B-cells (surface Immunoglobulins). The majority of these null cells are **Natural Killer (NK) cells**, which are identified by markers such as CD16 and CD56. In a healthy individual, the distribution of peripheral lymphocytes is approximately: * **T-cells:** 60–70% [1] * **B-cells:** 10–20% [1] * **Null cells (NK cells):** 10–15% [1] **Analysis of Options:** * **Option C (10-15%):** This is the correct physiological range for null cells in the peripheral blood. * **Option A (0-1%):** This value is too low; it might represent rare progenitor cells but does not account for the significant NK cell population. * **Option B (5-10%):** While closer, this underestimates the standard clinical range (10-15%) cited in major pathology textbooks like Robbins. * **Option D (15-20%):** This range overlaps more closely with the B-cell population rather than null cells. **High-Yield Clinical Pearls for NEET-PG:** * **NK Cell Function:** Unlike T and B cells, NK cells are part of the **innate immune system** and do not require prior sensitization. * **MHC Restriction:** NK cells are **not MHC-restricted**. They kill cells that show "missing self" (downregulation of MHC Class I), a common tactic used by viruses and tumors. * **Markers:** For MCQ purposes, remember **CD16** (FcγRIII) and **CD56** as the definitive markers for NK cells. * **Large Granular Lymphocytes (LGLs):** Morphologically, null cells often appear as LGLs in peripheral smears. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 579-580.

Question 97: Which type of hypersensitivity reaction is Rh incompatibility?

A. Type 1 hypersensitivity reaction
B. Type 2 hypersensitivity reaction (Correct Answer)
C. Type 3 hypersensitivity reaction
D. Type 4 hypersensitivity reaction

Explanation: **Explanation:** **Type 2 hypersensitivity reaction** is the correct answer because it involves **antibody-mediated cytotoxicity** [2]. In Rh incompatibility (Hemolytic Disease of the Newborn), maternal IgG antibodies are formed against the Rh (D) antigen present on the surface of fetal Red Blood Cells (RBCs) [3]. These antibodies cross the placenta, bind to the fetal RBCs, and lead to their destruction via opsonization and phagocytosis in the fetal spleen or through complement-mediated lysis [1], [2]. **Analysis of Incorrect Options:** * **Type 1 (Immediate):** Mediated by IgE antibodies and mast cell degranulation (e.g., Anaphylaxis, Asthma). Rh incompatibility does not involve IgE. * **Type 3 (Immune-complex):** Caused by the deposition of antigen-antibody complexes in tissues, leading to complement activation (e.g., SLE, Post-streptococcal glomerulonephritis). * **Type 4 (Delayed):** A cell-mediated response involving T-lymphocytes and macrophages, not antibodies (e.g., Mantoux test, Contact dermatitis). **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Type 2 reactions are "tissue-specific." Antigens are fixed on the cell surface (RBCs in this case) [2]. * **Coombs Test:** The **Indirect Coombs Test** is used to detect Rh antibodies in the maternal serum, while the **Direct Coombs Test** detects antibodies already bound to the neonate's RBCs. * **Prophylaxis:** Administering **Anti-D (RhoGAM)** to an Rh-negative mother at 28 weeks and within 72 hours of delivery prevents primary sensitization by clearing fetal RBCs from maternal circulation [1]. * **Other Type 2 Examples:** Myasthenia Gravis, Goodpasture Syndrome, Graves' Disease, and Autoimmune Hemolytic Anemia (AIHA) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 469-470. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 214. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 627-628.

Question 98: Human leukocyte antigen (HLA), which plays an important role in graft rejection, is present on which chromosome?

A. Short arm of chromosome 6 (Correct Answer)
B. Long arm of chromosome 6
C. Short arm of chromosome 3
D. Long arm of chromosome 3

Explanation: The **Human Leukocyte Antigen (HLA)** system is the human version of the **Major Histocompatibility Complex (MHC)**. These genes encode surface glycoproteins that are essential for the immune system to distinguish "self" from "non-self," making them the primary determinants of graft rejection in organ transplantation [1]. 1. **Why Option A is correct:** The HLA gene complex is located on the **short arm (p arm)** of **Chromosome 6** (specifically at 6p21.3) [2]. This region contains over 200 genes, including those for HLA Class I (A, B, C), Class II (DP, DQ, DR), and Class III (complement components like C2, C4, and TNF). 2. **Why Options B, C, and D are incorrect:** * **Long arm of chromosome 6:** While chromosome 6 contains the HLA complex, it is strictly localized to the short arm, not the long (q) arm. * **Chromosome 3:** This chromosome is not associated with the HLA complex. However, it is clinically significant in pathology for the **VHL (Von Hippel-Lindau) gene**, located on 3p. **High-Yield Clinical Pearls for NEET-PG:** * **MHC Class I (A, B, C):** Present on all nucleated cells and platelets (not on mature RBCs). They present endogenous antigens to **CD8+ T cells** [2]. * **MHC Class II (DP, DQ, DR):** Present only on **Antigen-Presenting Cells (APCs)** like macrophages, B-cells, and dendritic cells [2]. They present exogenous antigens to **CD4+ T cells**. * **Beta-2 Microglobulin:** While the heavy chains of HLA are on Chromosome 6, the $\beta$2-microglobulin component of Class I molecules is encoded on **Chromosome 15**. * **Haplotype:** HLA genes are codominantly expressed and inherited as a "haplotype" (one set from each parent). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 239-241. [2] 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. 156-157.

Question 99: What is the hallmark of AIDS in terms of cell count reduction?

A. CD3
B. CD4 (Correct Answer)
C. CD8
D. CD20

Explanation: **Explanation:** The hallmark of Human Immunodeficiency Virus (HIV) infection and its progression to AIDS is the progressive depletion of **CD4+ T-helper cells** [1]. **1. Why CD4 is correct:** The HIV virus specifically targets cells expressing the CD4 molecule on their surface. The viral envelope glycoprotein **gp120** binds to the **CD4 receptor**, along with co-receptors (CCR5 or CXCR4), to enter the cell. Once inside, the virus replicates, leading to cell death via cytolysis, apoptosis, or pyroptosis. A decline in the absolute CD4 count (typically below **200 cells/mm³**) is the defining laboratory criterion for AIDS, leading to profound immunosuppression and opportunistic infections [1]. **2. Why other options are incorrect:** * **CD3:** This is a pan-T-cell marker found on all T-lymphocytes (both CD4 and CD8). While the total CD3 count may drop as CD4 cells disappear, it is not the specific hallmark used to monitor disease progression. * **CD8:** These are cytotoxic T-cells. In early HIV infection, CD8 counts often *increase* as the body attempts to fight the virus. The **CD4:CD8 ratio**, which is normally 2:1, becomes **inverted** (<1:1) in AIDS [2]. * **CD20:** This is a marker for B-lymphocytes. HIV does not primarily infect or deplete B-cells, although it causes B-cell dysregulation and hypergammaglobulinemia. **Clinical Pearls for NEET-PG:** * **Normal CD4:CD8 ratio:** ~2:1. In AIDS, it is **inverted** [2]. * **CCR5 Mutation:** Individuals with a homozygous **CCR5-Δ32 mutation** are resistant to HIV infection. * **Indicator of Prognosis:** CD4 count is the best indicator of **immune status**, while Viral Load (HIV RNA) is the best predictor of **disease progression** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 256-260. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 555-556.

Question 100: Which of the following is a pan-leukocyte marker?

A. CD19
B. CD3
C. CD45 (Correct Answer)
D. CD45 RO

Explanation: **Explanation:** **CD45**, also known as the **Leukocyte Common Antigen (LCA)**, is a transmembrane protein tyrosine phosphatase essential for T and B cell receptor signaling. It is expressed on the surface of **all hematopoietic cells** (except mature erythrocytes and platelets), making it the definitive **pan-leukocyte marker**. In histopathology, immunohistochemistry (IHC) for CD45 is the primary tool used to differentiate undifferentiated malignant tumors of lymphoid origin (lymphomas) from carcinomas or sarcomas. **Analysis of Incorrect Options:** * **CD19:** This is a specific marker for **B-lymphocytes** [1]. It is expressed from the early stages of B-cell development until the plasma cell stage, making it a pan-B cell marker, not a pan-leukocyte marker [1]. * **CD3:** This is the definitive marker for **T-lymphocytes** [1]. It is part of the T-cell receptor (TCR) complex and is used to identify cells of T-lineage [1]. * **CD45 RO:** This is a specific isoform of CD45. While CD45 is the broad marker, the "RO" isoform is specifically expressed on **memory T-cells** and a subset of B-cells/monocytes. It is not universal to all leukocytes. **High-Yield Clinical Pearls for NEET-PG:** * **CD45 (LCA):** If a biopsy is "LCA positive," the diagnosis is almost certainly a **Lymphoma**. * **CD34:** Marker for hematopoietic **stem cells** (used in leukemia diagnosis). * **CD15 & CD30:** Classic markers for **Reed-Sternberg cells** in Hodgkin Lymphoma (except the lymphocyte-predominant type). * **CD68:** Marker for **Macrophages/Monocytes**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 598.

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