Increased susceptibility to N. meningitidis infections is associated with deficiency of which complement component:
Raji cell assays are used to quantitate
Which of the following statements is true about MHC class II?
Tuberculin test screens for
Which of the following is not true about innate immunity
C-C beta chemokines include
Tuberculin test positivity indicates -
Antigen presented along with HLA-II stimulates
Which of the following is NOT true about the lepromin test?
Which of the following complement components acts as a chemoattractant?
Explanation: ***C5-C9 deficiency*** - Deficiencies in **C5-C9 components** impair the formation of the **Membrane Attack Complex (MAC)**, which is crucial for lysing Gram-negative bacteria like **N. meningitidis**. - Patients with MAC deficiencies are at significantly higher risk for recurrent invasive **N. meningitidis** infections. *C1-C4 deficiency* - Deficiencies in **C1-C4 components** primarily affect the **classical complement pathway** and are associated with increased susceptibility to **bacterial infections** and **immune complex diseases** (e.g., SLE). - While these deficiencies compromise opsonization and inflammation, they are not specifically linked to recurrent **N. meningitidis** infections. *C3 deficiency* - **C3 deficiency** is a severe primary immunodeficiency leading to profound defects in complement activation via all pathways, affecting **opsonization** and the formation of the MAC. - This deficiency causes severe recurrent **pyogenic infections** due to encapsulated bacteria but is not as specifically or commonly linked to **N. meningitidis** as deficiencies in the terminal pathway. *C2 deficiency* - **C2 deficiency** is the most common complement deficiency and primarily impacts the **classical pathway**, leading to impaired opsonization and immune complex clearance. - It is often associated with recurrent infections (especially with encapsulated bacteria) and **lupus-like syndromes**, but not specifically increased susceptibility to **N. meningitidis** infections.
Explanation: ***Immune complexes*** - The Raji cell assay is a laboratory technique specifically designed to detect and quantify **circulating immune complexes** in serum. - Raji cells are a human lymphoblastoid cell line that expresses receptors for the Fc portion of IgG (FcγR) and complement components, allowing them to bind to and facilitate the detection of antigen-antibody complexes. *T cells* - **T cells** are a type of lymphocyte involved in cell-mediated immunity; their quantity is typically assessed using techniques like flow cytometry with specific cell markers (e.g., CD3, CD4, CD8). - Raji cell assays do not directly measure the absolute number or function of T cells. *Interferon level* - **Interferons** are cytokines with antiviral and immunomodulatory properties; their levels are usually measured using immunoassays such as ELISA (Enzyme-Linked Immunosorbent Assay). - The Raji cell assay is not designed to quantify interferon levels. *Complement level* - **Complement levels** (e.g., C3, C4, CH50) are typically assessed using immunoturbidimetric assays, nephelometry, or functional assays that measure complement activity. - While Raji cells express complement receptors, the assay primarily focuses on binding immune complexes, not direct quantification of complement proteins themselves.
Explanation: ***Not involved in innate immunity*** - **MHC class II molecules** are primarily involved in the **adaptive immune response**, presenting processed exogenous antigens to **helper T cells (CD4+)**. - Their function is to initiate a **specific and memory-driven immune response**, which is a hallmark of adaptive immunity, not innate immunity. *Cytotoxic T cells are involved* - **Cytotoxic T cells (CD8+)** recognize antigens presented by **MHC class I molecules**, which display endogenous peptides. - MHC class II molecules present antigens to **helper T cells (CD4+)**, which then coordinate the immune response. *Present only in B cells* - While **B cells** are important antigen-presenting cells that express MHC class II, they are not the only cells to do so. - **Macrophages** and **dendritic cells** are also professional antigen-presenting cells (APCs) that constitutively express MHC class II molecules. *Present in all nucleated cells* - **MHC class I molecules** are found on nearly all nucleated cells, presenting endogenous peptides to CD8+ T cells. - **MHC class II molecules** are restricted to professional antigen-presenting cells (APCs) like **dendritic cells, macrophages, and B cells**.
Explanation: ***Cell mediated immunity*** - The tuberculin test, or **Mantoux test**, assesses cell-mediated immunity by introducing **tuberculin purified protein derivative (PPD)** into the skin. - A positive reaction indicates a **delayed-type hypersensitivity (Type IV) reaction**, mediated by **T-lymphocytes** that have previously been sensitized to *Mycobacterium tuberculosis* antigens. *Complement function* - Complement function is assessed by tests like **CH50** or **AH50**, which measure the overall activity of the classical or alternative complement pathways, respectively. - These tests evaluate the ability of complement proteins to lyse target cells, not T-cell responses. *Humoral immunity* - Humoral immunity involves **B lymphocytes** and **antibodies**, which are assessed by measuring immunoglobulin levels (e.g., IgG, IgM, IgA) or specific antibody titers. - The tuberculin test does not directly measure antibody production or B-cell function. *Phagocyte dysfunction* - Phagocyte dysfunction is evaluated by tests such as the **nitroblue tetrazolium (NBT) test** or **dihydrorhodamine (DHR) test**, which assess the respiratory burst activity of neutrophils. - These tests are used to diagnose conditions like **chronic granulomatous disease** and do not involve delayed-type hypersensitivity reactions.
Explanation: ***Memory is seen*** - Innate immunity is characterized by a **lack of immunological memory**, meaning it does not \"remember\" previous encounters with pathogens to mount a stronger, faster response. - This feature is a hallmark of **adaptive (acquired) immunity**, which develops memory cells after initial exposure. *It is relatively non specific* - Innate immune responses are **non-specific** and target broad categories of pathogens, rather than specific antigens. - It recognizes conserved structures on pathogens, known as **Pathogen-Associated Molecular Patterns (PAMPs)**, shared by many different microbes. *It is first line of defence* - Innate immunity serves as the **body's immediate and primary defense** against invading pathogens. - It provides rapid protection through physical barriers, cellular components, and soluble factors, often preventing infection before it takes hold. *It is present prior to antigenic exposure* - The components of innate immunity are **pre-existing and fully functional** before any exposure to pathogens or antigens. - This readiness allows for an **instantaneous response** upon microbial invasion, without requiring prior sensitization.
Explanation: ***Eotaxin*** - **Eotaxin** (CCL11, CCL24, CCL26) is a key **C-C chemokine** that primarily attracts **eosinophils** to sites of allergic inflammation. - C-C chemokines are characterized by having two adjacent cysteine residues (CC) near the N-terminus. *IL-8* - **IL-8** (CXCL8) is a **C-X-C chemokine**, meaning it has an amino acid residue separating the first two cysteines (CXC motif). - Its primary role is to act as a potent **neutrophil chemoattractant** and activator. *Fractalkine* - **Fractalkine** (CX3CL1) is a unique chemokine belonging to the **C-X3-C chemokine** family, characterized by three amino acids separating the first two cysteines (CX3C motif). - It exists as both a **soluble chemokine** and a **membrane-bound molecule** involved in cell adhesion and leukocyte trafficking. *Lymphotactin* - **Lymphotactin** (XCL1) is a member of the **C chemokine (or XC chemokine)** family, distinguished by having only one cysteine residue at the N-terminus. - It is primarily involved in the chemotaxis of **T cells** and **NK cells**.
Explanation: ***Good cell-mediated immunity*** - A positive tuberculin test (Mantoux test) indicates the presence of **functional cell-mediated immunity** with **memory T cells** that recognize tuberculous antigens - This demonstrates a **delayed-type hypersensitivity (Type IV) reaction** mediated by **sensitized T lymphocytes** - The test confirms that the individual has a functioning **cell-mediated immune system** capable of mounting an immune response to mycobacterial antigens - **Important note**: A positive test shows the *presence* of CMI response to prior exposure, though it doesn't quantify the overall strength of immunity *Infection with Mycobacterium* - While a positive tuberculin test indicates **prior exposure or infection** with *Mycobacterium tuberculosis*, BCG vaccination, or non-tuberculous mycobacteria, the test specifically *measures* the **cell-mediated immune response** to this exposure - The test does not distinguish between **latent infection, active disease, or past exposure** - The question asks what the test "indicates" in immunological terms, which is the **presence of cell-mediated immunity**, rather than just infection status *Good humoral immunity* - The tuberculin test evaluates **cell-mediated immunity (Type IV hypersensitivity)**, not humoral immunity (antibody-mediated) - Humoral immunity involves **B cells and antibodies**, while the Mantoux test depends on **T cell-mediated responses** - Protection against *Mycobacterium tuberculosis* primarily requires cell-mediated immunity *None of the options* - This is incorrect because the tuberculin test directly demonstrates the **integrity and functionality of cell-mediated immunity** - The test's fundamental principle is detection of **memory T cells** that have been sensitized to mycobacterial antigens
Explanation: ***CD4 cells*** - Antigen presented with **MHC class II molecules** (formerly HLA-II) on antigen-presenting cells (APCs) is recognized by the **T-cell receptor (TCR)** on **CD4+ T helper cells**. - This interaction is crucial for the activation and differentiation of CD4+ T cells, leading to cytokine production and the coordination of the adaptive immune response. *CD2 cells* - **CD2** is a surface molecule found predominantly on T cells and NK cells, involved in cell adhesion and co-stimulation but not directly in the primary antigen recognition with MHC class II. - While CD2 plays a role in T cell activation, it does not directly recognize antigen presented via MHC class II. *CD8 cells* - **CD8+ T cells** (cytotoxic T lymphocytes) primarily recognize antigens presented by **MHC class I molecules**, which display intracellular (endogenous) antigens. - MHC class I presentation signals to CD8 cells to induce apoptosis in infected or cancerous cells. *CD19 cells* - **CD19** is a cell surface marker found on **B lymphocytes** and is involved in B cell activation and signaling. - B cells can act as APCs and present antigen, but their primary recognition of antigen is typically through their B-cell receptor (BCR), and they are not themselves stimulated by MHC class II in the same manner as T cells.
Explanation: ***It is diagnostic*** - The **lepromin test** is a measure of **cell-mediated immunity** to *Mycobacterium leprae* and is primarily used for **classification of leprosy**, not for diagnosing the disease itself. - A positive reaction indicates a robust immune response, characteristic of **tuberculoid leprosy**, while a negative reaction is seen in **lepromatous leprosy**. *Used to classify* - The lepromin test helps to **classify the type of leprosy** a patient has, differentiating between **tuberculoid** (positive reaction) and **lepromatous** (negative reaction) forms. - This classification is crucial for understanding the **patient's immune response** and prognosis. *BCG vaccination may convert negative to positive* - **BCG vaccination** can induce a mild, temporary **cell-mediated immune response** to mycobacterial antigens, which may result in a positive lepromin test in some individuals. - This cross-reactivity is due to the shared antigens between *Mycobacterium bovis* (used in BCG) and *Mycobacterium leprae*. *Negative in infants < 6 months* - Infants typically have a **developing immune system** and may not mount a strong cell-mediated immune response to lepromin, leading to a negative result. - This is similar to the **negative PPD test** often observed in very young infants even after BCG vaccination or exposure to tuberculosis due to their immature immune response.
Explanation: ***Correct: C5a*** - **C5a** is a powerful **chemoattractant** for neutrophils, monocytes, and macrophages, guiding them to sites of infection and inflammation. - It also acts as an **anaphylatoxin**, promoting inflammation through mast cell degranulation and histamine release. *Incorrect: C3b* - The primary function of **C3b** is **opsonization**, marking pathogens for phagocytosis by immune cells. - It also plays a crucial role in forming the **C5 convertase** in the complement activation pathways. *Incorrect: C4a* - **C4a** is a weak **anaphylatoxin** involved in modulating inflammation, but its chemotactic activity is minimal. - It is generated during the activation of the **classical** and **lectin pathways** of complement. *Incorrect: C3a* - **C3a** is an **anaphylatoxin** that promotes inflammation by inducing degranulation of mast cells and basophils. - It has some weak chemotactic properties but is considerably less potent than **C5a** in attracting immune cells.
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