Immunology & Medical Microbiology - Innate Immunity, Pathogens & Antibodies Flashcards

Question 1

What is the primary role of the complement system in innate immunity?

Accepted Answer

The complement system is a group of plasma proteins that, when activated, enhances (complements) the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen's cell membrane.

Question 2

Describe the activation of the Classical Complement Pathway.

Accepted Answer

Activated primarily by antibody-antigen complexes (IgG or IgM bound to antigen) or directly by C-reactive protein. C1 complex (C1q, C1r, C1s) binds to the Fc region of antibodies, leading to activation of C1r and C1s, which then cleave C4 and C2 to form C3 convertase ($C4b2a$).

Question 3

Describe the activation of the Lectin Complement Pathway.

Accepted Answer

Activated when Mannose-binding Lectin (MBL) or ficolins bind to specific carbohydrate patterns (e.g., mannose) on microbial surfaces. MBL is associated with MASP-1 and MASP-2 (MBL-associated serine proteases), which then cleave C4 and C2 to form C3 convertase ($C4b2a$), similar to the classical pathway.

Question 4

Describe the activation of the Alternative Complement Pathway.

Accepted Answer

Activated spontaneously by "tickover" of C3 in plasma, which is then stabilized by microbial surfaces (e.g., LPS, teichoic acids) and factor B and factor D. This forms the alternative C3 convertase ($C3bBb$). Properdin stabilizes this convertase, amplifying the pathway.

Question 5

What are the main effector functions of the activated complement system?

Accepted Answer

1. **Opsonization:** C3b coats pathogens, enhancing phagocytosis.
2. **Inflammation:** C3a and C5a (anaphylatoxins) recruit phagocytes and promote inflammation.
3. **Cell Lysis:** Formation of the Membrane Attack Complex (MAC) by C5b-C9, creating pores in microbial membranes.

Question 6

Characterize Immunoglobulin G (IgG).

Accepted Answer

*   **Structure:** Monomer.
*   **Location:** Most abundant Ig in serum, crosses placenta, found in extravascular spaces.
*   **Functions:** Primary antibody in secondary immune response, opsonization, complement activation (classical), antibody-dependent cell-mediated cytotoxicity (ADCC), neonatal immunity (passive).

Question 7

Characterize Immunoglobulin A (IgA).

Accepted Answer

*   **Structure:** Monomer in serum, Dimer (secretory IgA) in secretions (joined by J chain and secretory component).
*   **Location:** Mucosal secretions (saliva, tears, breast milk, gut, respiratory tract).
*   **Functions:** Mucosal immunity, neutralizes toxins and pathogens, prevents adherence of microbes to epithelial surfaces.

Question 8

Characterize Immunoglobulin M (IgM).

Accepted Answer

*   **Structure:** Pentamer in serum (joined by J chain), monomer on B cell surface (as B cell receptor).
*   **Location:** Primarily in blood and lymph.
*   **Functions:** Primary antibody in primary immune response, potent complement activator (classical), B cell receptor.

Question 9

Characterize Immunoglobulin E (IgE).

Accepted Answer

*   **Structure:** Monomer.
*   **Location:** Low concentration in serum, primarily bound to Fc receptors on mast cells and basophils.
*   **Functions:** Mediates Type I hypersensitivity reactions (allergies), defense against parasites (helminths).

Question 10

Characterize Immunoglobulin D (IgD).

Accepted Answer

*   **Structure:** Monomer.
*   **Location:** Primarily found on the surface of naive B cells (co-expressed with IgM).
*   **Functions:** Acts as a B cell receptor, involved in B cell activation and differentiation, but its exact role is less understood compared to other Ig classes.

Question 11

Describe Type I Hypersensitivity (Anaphylactic/Immediate).

Accepted Answer

*   **Mechanism:** IgE-mediated. Allergen exposure leads to IgE production, which binds to Fc receptors on mast cells and basophils. Subsequent exposure causes cross-linking of IgE, triggering degranulation and release of histamine, leukotrienes, and prostaglandins.
*   **Examples:** Allergic rhinitis, asthma, anaphylaxis, food allergies.

Question 12

Describe Type II Hypersensitivity (Cytotoxic).

Accepted Answer

*   **Mechanism:** Antibody-mediated (IgG or IgM). Antibodies bind to antigens on the surface of cells, leading to cell destruction via complement activation, ADCC, or opsonization.
*   **Examples:** Hemolytic disease of the newborn, transfusion reactions, autoimmune hemolytic anemia, Goodpasture's syndrome.

Question 13

Describe Type III Hypersensitivity (Immune Complex).

Accepted Answer

*   **Mechanism:** Immune complex-mediated. Soluble antigen-antibody complexes (IgG or IgM) form in the blood, deposit in tissues (e.g., blood vessel walls, glomeruli), and activate complement, leading to inflammation and tissue damage.
*   **Examples:** Serum sickness, Arthus reaction, Systemic Lupus Erythematosus (SLE), post-streptococcal glomerulonephritis.

Question 14

Describe Type IV Hypersensitivity (Delayed-Type Hypersensitivity, DTH).

Accepted Answer

*   **Mechanism:** T cell-mediated (not antibody-mediated). Sensitized T cells (CD4+ Th1 or CD8+ cytotoxic T cells) respond to antigens, releasing cytokines that activate macrophages and induce inflammation and tissue damage. Reaction develops 24-72 hours after antigen exposure.
*   **Examples:** Contact dermatitis (e.g., poison ivy), tuberculin skin test, graft rejection, multiple sclerosis.

Question 15

What are the key structural features of a Gram-positive bacterial cell wall?

Accepted Answer

*   **Thick Peptidoglycan Layer:** Multiple layers of peptidoglycan (murein).
*   **Teichoic Acids & Lipoteichoic Acids:** Polymers embedded in the peptidoglycan, extending to the cell surface, contributing to antigenicity and virulence.
*   **No Outer Membrane:** Lacks an outer membrane.
*   **Periplasmic Space:** Very small or absent.

Question 16

What are the key structural features of a Gram-negative bacterial cell wall?

Accepted Answer

*   **Thin Peptidoglycan Layer:** A single layer of peptidoglycan.
*   **Outer Membrane:** Present, containing Lipopolysaccharide (LPS), porins, and other proteins.
*   **Lipopolysaccharide (LPS):** Composed of O-antigen, core polysaccharide, and Lipid A (endotoxin).
*   **Periplasmic Space:** Large, containing enzymes and transport proteins.

Question 17

What is the clinical significance of Lipopolysaccharide (LPS) in Gram-negative bacteria?

Accepted Answer

LPS, specifically its Lipid A component, acts as a potent endotoxin. When released (e.g., during bacterial lysis), it can trigger a strong inflammatory response, leading to fever, septic shock, disseminated intravascular coagulation (DIC), and multi-organ failure.

Question 18

How are B cells typically activated to produce antibodies (T-dependent activation)?

Accepted Answer

Naive B cells bind to their specific antigen via the B cell receptor (BCR), internalize it, and present processed peptides on MHC Class II molecules. A helper T cell (CD4+ T cell) that recognizes the same peptide-MHC II complex provides co-stimulation (e.g., CD40-CD40L interaction) and cytokines, leading to B cell proliferation, differentiation into plasma cells (antibody production), and memory B cells.

Question 19

Describe the two main pathways for T cell activation.

Accepted Answer

1.  **CD4+ Helper T cells:** Activated by antigen presented on MHC Class II molecules (found on APCs like dendritic cells, macrophages, B cells). Requires co-stimulation (e.g., CD28-B7).
2.  **CD8+ Cytotoxic T cells:** Activated by antigen presented on MHC Class I molecules (found on all nucleated cells). Requires co-stimulation and often help from CD4+ T cells.

Question 20

What is the role of MHC Class I molecules in T cell activation?

Accepted Answer

MHC Class I molecules present endogenous antigens (peptides derived from proteins synthesized within the cell, e.g., viral proteins, tumor antigens) to CD8+ cytotoxic T lymphocytes (CTLs). This interaction signals to the CTL that the cell is infected or abnormal, leading to its destruction.

Question 21

What is the role of MHC Class II molecules in T cell activation?

Accepted Answer

MHC Class II molecules present exogenous antigens (peptides derived from proteins taken up by phagocytosis or endocytosis, e.g., bacterial proteins) to CD4+ helper T lymphocytes. This interaction activates helper T cells, which then orchestrate immune responses by releasing cytokines and helping B cells and CD8+ T cells.

Question 22

Briefly explain the function of CD4+ Helper T cells.

Accepted Answer

CD4+ Helper T cells recognize antigens presented on MHC Class II molecules. Upon activation, they differentiate into various subsets (e.g., Th1, Th2, Th17, Treg) and secrete cytokines that orchestrate and regulate immune responses, including activating B cells, macrophages, and CD8+ T cells.

Question 23

Briefly explain the function of CD8+ Cytotoxic T cells.

Accepted Answer

CD8+ Cytotoxic T cells (CTLs) recognize antigens presented on MHC Class I molecules. Upon activation, they directly kill target cells (e.g., virus-infected cells, tumor cells) by inducing apoptosis through mechanisms involving perforin and granzymes, or Fas-FasL interaction.

Immunology & Medical Microbiology - Innate Immunity, Pathogens & Antibodies

Cards in this deck

Related Flashcard Sets

JLPT N2 - Upper-Intermediate Japanese Kanji, Grammar & Expressions

CompTIA Network+ (N10-008) - Networking Fundamentals & Subnetting

HSK 4 - Intermediate Chinese Vocabulary & Grammar

CompTIA Network+ (N10-008) - Networking Fundamentals & Protocols