Which of the following is not considered an antigen-presenting cell?
A 32 year old man presents with a 3-month history of weight loss, night sweats, a productive cough with blood-tinged sputum, anorexia, general malaise, and a low grade fever. A PPD skin test shows > 10 mm of induration. If the area of induration were biopsied, which of the following type of reactive cells would be found?
IgE is secreted by which of the following cells?
Which immunoglobulin is most efficient at fixing C1q in the classical complement pathway?
Which type of hypersensitivity is associated with cell-mediated immunity?
MHC II is associated with:-
Affinity maturation of antibodies is because of _____ .
CD3 is a marker for which type of cells?
Which of the following is not a component of innate immunity?
The process by which antigen-specific B lymphocytes are selected and activated to proliferate and produce antibodies is called:
Explanation: ***Thymocytes*** - Thymocytes are **developing T cells** found in the thymus and do not function as antigen-presenting cells (APCs) [1]. - Unlike APCs, thymocytes are primarily involved in the **maturation** and selection of T lymphocytes. *Langerhans cells* - Langerhans cells are a type of **dendritic cell** found in the skin and are effective antigen-presenting cells to T cells [1]. - They play a crucial role in **immune surveillance** and response to skin infections. *Macrophages* - Macrophages are well-known antigen-presenting cells that engulf pathogens and present antigens to T cells [1]. - They are also involved in **phagocytosis** and secrete various cytokines to modulate immune responses. *M-cells* - M-cells (microfold cells) are specialized epithelial cells that transport antigens from the intestinal lumen to underlying immune cells. - Although not traditional APCs, they play a role in immune surveillance and stimulating **mucosal immunity**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 200, 207-208.
Explanation: ***T lymphocyte*** - The clinical picture (weight loss, night sweats, productive cough with blood-tinged sputum, positive PPD) is highly suggestive of **tuberculosis**, a **Type IV hypersensitivity reaction** [1], [2]. - **Type IV hypersensitivity reactions** are cell-mediated, involving the activation of **T lymphocytes**, which migrate to the site of antigen exposure (like a PPD test site or a tuberculous granuloma) and release cytokines, leading to induration and inflammation [1], [2]. *Eosinophil* - **Eosinophils** are primarily involved in allergic reactions and defense against parasitic infections [3]. - They are not the predominant reactive cells in a **Type IV hypersensitivity** response like that seen in tuberculosis [1]. *Mast cell* - **Mast cells** play a critical role in immediate hypersensitivity reactions (Type I), releasing histamine and other mediators [4]. - They are not the primary cells involved in the delayed-type hypersensitivity response elicited by tuberculin purified protein derivative (PPD) [2]. *B lymphocyte* - **B lymphocytes** are responsible for humoral immunity by producing antibodies [3]. - While they contribute to overall immune responses, they are not the main effector cells in a cell-mediated **Type IV hypersensitivity reaction** characteristic of a positive PPD test [1], [2]. **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. 173-174. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 218. [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. 195-196. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210.
Explanation: ***Plasma cells*** - Plasma cells are **terminally differentiated B lymphocytes** that are specialized in producing and secreting large quantities of antibodies, including **IgE**. - While other cells like mast cells and basophils have receptors for IgE and play roles in IgE-mediated reactions, they do not synthesize **IgE** themselves. *Mast cell* - Mast cells are key players in allergic reactions and express **FcεRI receptors** that bind to IgE antibodies. - Upon binding the antigen, they degranulate, releasing **histamine** and other mediators, but they do not produce IgE. *Basophils* - Basophils also express **FcεRI receptors** for IgE and are involved in allergic responses, releasing inflammatory mediators. - Similar to mast cells, they do not synthesize IgE, but rather bind pre-formed **IgE** antibodies. *Eosinophils* - Eosinophils are involved in allergic reactions and defense against **parasitic infections**, and their granules contain toxic proteins. - They can be activated by IgE-mediated mechanisms but are not producers of **IgE** antibodies.
Explanation: ***IgM*** - **IgM** is the most efficient immunoglobulin at activating the **classical complement pathway** due to its pentameric structure, which provides multiple binding sites for C1q. - The **Fc portion** of IgM, when bound to an antigen, undergoes a conformational change that exposes binding sites for the **C1q component** of complement. *IgA* - **IgA** primarily functions in **mucosal immunity** and does not efficiently activate the classical complement pathway. - It can weakly activate the **alternative complement pathway** but is not known for fixing C1. *IgG* - **IgG** can activate the classical complement pathway, but it requires two or more IgG molecules to be in close proximity on the cell surface to effectively bind C1q, making it less efficient than IgM. - Its **Fc region** binds C1q only when **antigen-antibody complexes** are formed, but it's not the primary immunoglobulin for initiating C1 binding in solitary form. *IgE* - **IgE** is primarily involved in **allergic reactions** and defense against parasites, binding to Fc receptors on mast cells and basophils. - It does **not activate the complement system** via the classical pathway and therefore does not fix C1.
Explanation: ***Type 4*** - Cell-mediated immunity primarily involves **T-lymphocytes** [1], essential for targeting and eliminating **intracellular pathogens** like viruses. - It plays a crucial role in **delayed-type hypersensitivity reactions** [2], making it vital for the adaptive immune response. *Type 3* - Type 3 immune responses are primarily associated with **immune complex-mediated** diseases and not directly with cell-mediated immunity. - This type involves primarily **B-cells** and antibodies in the response against antigens. *Type 2* - Type 2 immunity mainly concerns the activation of **B-lymphocytes** and antibody production against **extracellular pathogens** like bacteria. - It is characterized by **IgE-mediated responses** [3], particularly in allergic reactions, rather than cell-mediated actions. *Type 1* - Type 1 responses are associated with **Th1 cells** [2] and are more specifically linked to **autoimmunity and cell-mediated pathways**, but represent only a part of the broader cell-mediated immunity. - This type mainly focuses on clearance of **intracellular pathogens** but is not synonymous with the entire process of cell-mediated immunity. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 207-208. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 216-218. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 208-210.
Explanation: ***Antigen presenting cells*** - **MHC II (Major Histocompatibility Complex class II)** molecules are primarily expressed on the surface of professional **antigen-presenting cells (APCs)**. - APCs, such as **macrophages**, **dendritic cells**, and **B lymphocytes**, use MHC II to present **extracellularly derived antigens** to **CD4+ T helper cells**. *Red blood cells* - **Red blood cells (RBCs)** are anucleated and lack MHC molecules entirely. - Their primary function is **oxygen transport**, not immune cell communication. *Platelets* - **Platelets** are cell fragments involved in **hemostasis** (blood clotting). - They do not express MHC class II molecules as they are not involved in antigen presentation. *Epithelial cells* - Most **epithelial cells** primarily express **MHC class I** molecules to present **intracellular antigens** to **CD8+ cytotoxic T cells**. - They do not typically express MHC class II unless under specific inflammatory conditions, and even then, not as their primary function.
Explanation: ***Somatic hypermutation*** - **Somatic hypermutation** is a process that introduces point mutations in the **variable regions** of immunoglobulin genes, primarily in B cells. - These mutations lead to the production of B cells with slightly altered **antibody affinities**, allowing for selection of those with higher affinity for the antigen. *Gene rearrangements* - **Gene rearrangements**, specifically **V(D)J recombination**, are responsible for the initial diversity of antibody specificities in immature B cells. - This process determines the basic antigen-binding site but does not fine-tune the **affinity** after initial antigen exposure. *CD40* - **CD40** is a co-stimulatory molecule on B cells that binds to **CD40L** on T cells, crucial for B cell activation, **isotype switching**, and germinal center formation. - While essential for antibody responses and germinal center reactions where affinity maturation occurs, **CD40** itself does not directly cause the molecular changes that lead to affinity maturation. *Differential mRNA processing* - **Differential mRNA processing** (or alternative splicing) primarily controls the production of different protein isoforms from a single gene. - In the context of antibodies, it can determine whether a B cell produces **membrane-bound** or **secreted** forms of antibodies, but it does not enhance the antigen-binding affinity.
Explanation: ***T - cells*** - **CD3** is a complex of proteins that is universally expressed on the surface of all **T lymphocytes** (T cells). - It plays a crucial role in **T cell activation** by transducing signals from the T cell receptor (TCR) to the cell's interior. *B - cells* - **B cells** are characterized by the expression of unique surface markers like **CD19**, **CD20**, and surface **immunoglobulins**, not CD3. - Their primary function is to produce **antibodies** and present antigens. *NK - cells* - **Natural Killer (NK) cells** are a type of lymphocyte that lacks both CD3 and a T cell receptor (TCR), differentiating them from T cells. - They express markers such as **CD16** and **CD56** and are involved in innate immunity, particularly against viral infections and tumor cells. *Monocytes* - **Monocytes** are myeloid cells, not lymphocytes, and are characterized by markers such as **CD14** and **CD68**. - They differentiate into macrophages and dendritic cells, playing a significant role in phagocytosis and antigen presentation.
Explanation: ***Helper T lymphocyte*** - Helper T lymphocytes are a crucial part of **adaptive immunity** [4], facilitating responses against pathogens. - They specifically activate B cells and cytotoxic T cells [2], unlike components of innate immunity, which respond nonspecifically. *NK cells* - Natural Killer (NK) cells are integral to **innate immunity** [1], targeting infected or tumor cells without prior sensitization. - They play a role in the initial response to viral infections and can produce **cytokines** [2]. *Epithelial barriers* - Epithelial barriers act as the first line of defense in **innate immunity** [1], preventing pathogen entry. - They include physical and chemical barriers like skin and mucous membranes [3]. *Dendritic cells* - Dendritic cells are key antigen-presenting cells involved in **innate immunity** [1] and link to adaptive immunity. - They capture and present antigens [2], activating T cells to mount an immune response. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 194-196. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 207-208. [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. 152-153. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 196-198.
Explanation: ***Clonal selection*** - **Clonal selection** is the fundamental process by which an antigen-specific B lymphocyte is **selected** when its B cell receptor (BCR) recognizes and binds to a matching antigen. - This binding triggers the B cell to become **activated**, **proliferate** (undergo clonal expansion), and **differentiate** into plasma cells that produce antibodies specific to that antigen. - This process is the cornerstone of **adaptive immunity**, ensuring that only B cells with receptors matching the encountered antigen are stimulated to respond. *Class switching* - **Class switching** (isotype switching) occurs AFTER clonal selection and activation. - It allows already-activated B cells to change the **antibody class** they produce (from IgM to IgG, IgA, or IgE) while maintaining the **same antigen specificity**. - This process modifies effector functions but does NOT involve the initial selection and activation of antigen-specific B cells. *Group switching* - This is not a recognized term in immunology. - It does not describe any standard process of B cell activation or antibody production. *Hybridisation* - **Hybridization** refers to the formation of double-stranded nucleic acids from complementary strands or the creation of hybrid cells (e.g., hybridomas for monoclonal antibody production). - It is not the physiological process by which B lymphocytes are selected and activated in response to antigen exposure.
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