Immunology Chapter on Inflammation and Hypersensitivity
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Questions and Answers

What is a common result of chronic inflammation?

  • Tissue remodeling (correct)
  • Production of antibodies
  • Increased blood flow
  • Pain and swelling

    • What is the main type of cell involved in chronic inflammation?

  • Neutrophils
  • Macrophages (correct)
  • Mast cells
  • Eosinophils

    • What is the primary function of mast cells in type I hypersensitivity reactions?

  • Activation of complement
  • Production of antibodies
  • Phagocytosis of antigens
  • Release of histamine and other inflammatory mediators (correct)

    • What is the key difference between type II and type III hypersensitivity reactions?

    <p>The involvement of complement (B)</p> Signup and view all the answers

    How do non-IgE dependent drug-induced hypersensitivity reactions occur?

    <p>Binding of the drug to circulating blood cells (A)</p> Signup and view all the answers

    Which of the following is NOT a component of the complement system?

    <p>Neutrophils (B)</p> Signup and view all the answers

    What is the function of MBL in the immune response?

    <p>Activates the classical pathway of complement activation. (A)</p> Signup and view all the answers

    Which of the following is TRUE about C3 deficiency?

    <p>It leads to a decreased ability to form the membrane attack complex (MAC). (A)</p> Signup and view all the answers

    Which of the following cells is NOT involved in the inflammatory response?

    <p>Red blood cells (B)</p> Signup and view all the answers

    Which of the following is a characteristic change observed during the inflammatory response?

    <p>Increased adhesiveness of leukocytes to the vascular endothelium. (D)</p> Signup and view all the answers

    What is the role of cytokines in inflammation?

    <p>They mediate the recruitment and activation of immune cells. (A)</p> Signup and view all the answers

    Which of the following statements regarding the complement system is TRUE?

    <p>It can be activated by the binding of C3 to microbial surface structures. (B)</p> Signup and view all the answers

    What is the primary function of the membrane attack complex (MAC)?

    <p>To directly kill microbes by forming pores in their cell membranes. (C)</p> Signup and view all the answers

    What is the primary function of the C3b complement component in the context of immune complexes?

    <p>C3b binds to immune complexes, acting as an opsonin and promoting phagocytosis. (A)</p> Signup and view all the answers

    What is the primary mechanism by which C5a contributes to tissue injury?

    <p>C5a recruits and activates leukocytes, which can cause tissue damage through the release of lytic enzymes. (A)</p> Signup and view all the answers

    Which of the following is NOT a direct consequence of complement activation?

    <p>Production of antibodies against the antigen causing the immune complex formation. (C)</p> Signup and view all the answers

    How do smaller immune complexes contribute to tissue damage differently from larger complexes?

    <p>Smaller complexes can pass through basement membranes and be deposited in tissues more easily. (B)</p> Signup and view all the answers

    Which of these complement components acts as an anaphylatoxin, causing mast-cell degranulation?

    <p>C5a (A)</p> Signup and view all the answers

    What is the primary reason why immune complexes can cause disease only when produced in excess?

    <p>Excess immune complexes overwhelm the body's ability to clear them effectively, allowing them to deposit in tissues. (D)</p> Signup and view all the answers

    How do immune complexes typically lead to tissue injury?

    <p>Triggering the release of inflammatory mediators, leading to leukocyte recruitment and tissue damage. (B)</p> Signup and view all the answers

    Which of the following sites is NOT a common location for immune complex deposition?

    <p>Lymph Nodes (A)</p> Signup and view all the answers

    Which of the following is NOT a direct effect of StrepSAgs on the immune system?

    <p>Direct activation of complement (B)</p> Signup and view all the answers

    What is the primary mode of transmission for Group A streptococcal pharyngitis?

    <p>Droplet transmission via coughing, sneezing, or conversation (B)</p> Signup and view all the answers

    What is the primary biological function of streptokinase produced by GAS?

    <p>Lysis of fibrin clots through plasminogen conversion (D)</p> Signup and view all the answers

    What is the typical latent period between a respiratory infection with Group A streptococci and the onset of poststreptococcal glomerulonephritis?

    <p>10 days (C)</p> Signup and view all the answers

    Which of the following statements accurately describes the role of C5a peptidase in the pathogenesis of GAS infections?

    <p>It degrades C5a, a chemoattractant for phagocytes, hindering host defense (C)</p> Signup and view all the answers

    What is the most common bacterial cause of pharyngitis in school-age children between 5 and 15 years old?

    <p>Group A streptococci (E)</p> Signup and view all the answers

    How does the superantigen mechanism of StrepSAgs contribute to the symptoms of GAS infection?

    <p>It induces excessive cytokine release, leading to inflammation and immune dysregulation (B)</p> Signup and view all the answers

    Which of the following is an accurate statement regarding the duration of GAS persistence in untreated pharyngitis?

    <p>GAS can persist for 1 to 4 weeks after the disappearance of pharyngitis symptoms. (B)</p> Signup and view all the answers

    Which of the following antimicrobial agents would be considered the LEAST effective against Group A streptococci?

    <p>Aminoglycosides (A)</p> Signup and view all the answers

    What is a potential consequence of inadequate treatment of streptococcal pharyngitis within 10 days of onset?

    <p>Development of rheumatic fever (C)</p> Signup and view all the answers

    What is the mechanism of action of the multivalent vaccines being developed to prevent Group A streptococcal infections?

    <p>Targeting of specific M protein epitopes that are not cross-reactive with the host (A)</p> Signup and view all the answers

    Which of the following statements about the treatment of Group A streptococcal infections is TRUE?

    <p>Treatment of acute infection can prevent the development of acute glomerulonephritis. (A)</p> Signup and view all the answers

    Which of the following is a reason why treating streptococcal pharyngitis is not a guaranteed cure?

    <p>The short course of the natural infection makes treatment less effective. (C)</p> Signup and view all the answers

    What type of cell are Group A Streptococci?

    <p>Spherical or Ovoid (D)</p> Signup and view all the answers

    What characterizes Group A Streptococci colonies on blood agar plates?

    <p>Small, compact colonies with a narrow zone of β-hemolysis (D)</p> Signup and view all the answers

    Which of the following is a characteristic of streptolysin O?

    <p>It is a pore-forming cytotoxin that lyses leukocytes, tissue cells, and platelets. (A)</p> Signup and view all the answers

    What is the primary mechanism by which immune complexes contribute to the development of systemic immunologic diseases?

    <p>Triggering the release of vasoactive mediators from leukocytes and mast cells (D)</p> Signup and view all the answers

    Which of the following is NOT a characteristic of the immune complex deposition in systemic immunologic diseases?

    <p>The antigens involved in immune complexes are always known and easily identifiable. (D)</p> Signup and view all the answers

    What is the mechanism of post-streptococcal glomerulonephritis?

    <p>Deposition of immune complexes containing streptococcal antigens in the glomeruli (C)</p> Signup and view all the answers

    What is a possible explanation for the presence of immune complexes in some forms of glomerulonephritis, even when they are not detected in circulation?

    <p>The antigens may first become embedded in the kidney tissue, and the immune complexes form locally. (C)</p> Signup and view all the answers

    What type of toxin is Streptolysin O, and what is its primary effect?

    <p>Pore-forming cytotoxin; lyses various cells (C)</p> Signup and view all the answers

    Signup and view all the answers

    Flashcards

    Acute Inflammation

    Rapid inflammatory response lasting from minutes to days.

    Chronic Inflammation

    Prolonged inflammation that follows acute inflammation if unresolved.

    Type I Hypersensitivity

    Immediate allergic reactions mediated by IgE antibodies.

    Cytokines

    Signaling proteins involved in local and systemic inflammation.

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    Phagocytosis

    Process by which cells engulf and destroy pathogens.

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    Alternative Pathway

    A complement activation pathway triggered by C3 recognition of microbial structures.

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    MBL (Mannose-Binding Lectin)

    A collectin protein that binds microbes and triggers complement activation.

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    MASP1 and MASP2

    Zymogens activated by MBL that initiate proteolytic steps in complement activation.

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    C3 Deficiency

    A condition causing increased susceptibility to recurrent bacterial infections.

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    MAC (Membrane Attack Complex)

    The terminal product of the classical pathway that lyses bacterial cells.

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    Neutrophils

    The most abundant leukocytes recruited to sites of acute inflammation.

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    Acute-Phase Reactants

    Plasma proteins that increase in response to inflammation and injury.

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    C5a Receptor

    A receptor on leukocytes activated by C5a in inflammation.

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    Anaphylatoxins

    C3a, C4a, and C5a induce mast-cell degranulation and increase permeability.

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    Opsonin

    C3b coats immune complexes to facilitate phagocytosis by neutrophils.

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    Immune Complex Deposition

    Accumulation of antigen-antibody complexes in tissues causing injury.

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    Neutrophil Activation

    Neutrophils respond to C3a and C5a, leading to tissue injury.

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    Microthrombi Formation

    Results from platelet aggregation induced by complement activation.

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    Basement Membrane

    A barrier where immune complexes deposit, impacting organs like kidneys.

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    Cationic Antigens

    Antigens that bind to negatively charged basement membranes, causing injury.

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    Group A Streptococci Treatment

    Penicillin G is the antimicrobial of choice for treating Group A streptococci infections.

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    Penicillin Allergy Alternatives

    Patients allergic to penicillin are treated with clindamycin or azithromycin.

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    Impetigo Treatment

    Clindamycin is often used to treat impetigo, covering for streptococcal infections.

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    Rheumatic Fever Prevention

    Adequate treatment of streptococcal pharyngitis within 10 days prevents rheumatic fever.

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    M Protein Vaccines

    Multivalent vaccines using M protein epitopes are in trials to prevent strep infections.

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    Systemic Lupus Erythematosus (SLE)

    An autoimmune disease causing immune complexes to deposit in various tissues.

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    Post-Streptococcal Glomerulonephritis

    A kidney disease from immune complexes formed after streptococcal infection.

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    Group A Streptococci

    A type of bacteria known for causing infections and producing toxins.

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    Beta-Hemolysis

    The complete lysis of red blood cells by bacterial toxins, observed on blood agar.

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    Streptolysin O

    A cytotoxin produced by Group A Streptococci that lyses host cells.

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    Streptococcal Superantigen Toxins

    Proteins that trigger extreme immune responses, leading to diseases like scarlet fever.

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    C5a Peptidase

    An enzyme made by Group A Streptococcus that degrades the C5a complement component.

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    Streptokinase

    An extracellular enzyme that lyses fibrin clots by converting plasminogen to plasmin.

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    Superantigens

    Proteins that can activate a large number of T-cells leading to cytokine release.

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    Group A Streptococci (GAS)

    Bacteria responsible for various infections, including pharyngitis and skin infections.

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    Pharyngitis

    An infection of the throat frequently caused by Group A Streptococcus in children.

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    ASO Test

    A serological test that quantifies antibodies against Streptolysin O.

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    Study Notes

    Cellular Immune Response in Kidney Disease

    • The presentation discusses the cellular immune response in kidney disease.
    • Pathogens are categorized into five groups: viruses, bacteria, fungi, protozoa, and helminths (worms).
    • Pathogens can be found in various body compartments, requiring different host defense mechanisms.

    Immune Response

    • Pathogen containment by anatomical barriers is a primary defense mechanism.
    • Early induced innate responses occur within 4-96 hours, targeting and removing infectious agents.
    • Adaptive immune responses occur after 96 hours.

    Anatomic Barriers and Initial Chemical Defenses

    • Pathogens cause disease and damage tissues.
    • Intracellular pathogens (e.g., viruses) are not accessible to initial defenses but are targeted by natural killer (NK) cells and cytotoxic T cells.
    • Macrophage activation by NK or T cells kills invading pathogens.

    Extracellular vs. Intracellular

    • Pathogens can be either extracellular (in interstitial spaces, blood, lymph, or on epithelial surfaces) or intracellular (cytoplasmic, vesicular).
    • Different protective immunities (complement, phagocytosis, antibodies) target extracellular and intracellular pathogens.

    Pathogens Can Damage Tissues

    • Various mechanisms of pathogen-induced tissue damage are presented.
    • Direct mechanisms, such as exotoxin production, endotoxin release, or direct cytopathic effects.
    • Indirect mechanisms, such as immune complexes, anti-host antibodies, or cell-mediated immunity.

    Complement Activation

    • The complement system is a key component of innate immunity.
    • Complement activation occurs in stages, starting with pattern recognition that triggers protease cascade amplification. These stages can lead to phagocytosis, inflammation, and membrane attack.

    Pathways of Complement Activation

    • Complement activation pathways are the alternative pathway, the classical pathway, and the lectin pathway.
    • Each pathway triggers complement cascade amplification leading to different effector functions including opsonization and inflammation.

    The Classical Pathway

    • The classical pathway is crucial in adaptive immunity's humoral arm.
    • The classical pathway is initiated by soluble proteins (pentraxins).
    • A complement component (MBL) is a member of the collectin family with a hexameric structure.

    Immune Complex Disease in Kidney

    • Pathological immune complex deposition in kidneys can cause disease.
    • Immune complexes, formed from antigen-antibody complexes, are deposited in small blood vessels.
    • Immune complexes activate complement, leading to inflammation and, in some instances, necrosis. (Severe and long-lasting tissue injury can result.)

    Immune Complex Diseases in Kidneys—Pathogenesis

    -   Nephritogenic strains are limited to a few M types and seem to have declined.
-   M protein of some nephritogenic strains share antigenic determinants with glomeruli.
-   The renal injury of acute glomerulonephritis is caused by immune complex deposition.

    Clinical Manifestations

    • The clinical course of post-streptococcal glomerulonephritis (PSGN) is often benign. There is spontaneous healing over weeks or months but occasionally, a course progresses to renal failure or death.

    Diagnosis

    • Detecting group A antigen directly from throat swabs is a widely available diagnostic tool.
    • Several serological tests were developed to support the diagnosis of PSGN.

    Treatment

    -   Penicillin G is the antimicrobial of choice for Group A streptococcal infection.
-   Alternative antibacterials may be used for patients with penicillin allergies.

    Prevention

    • Multivalent vaccines utilizing M protein epitopes are being explored in clinical trials as a prevention measure.

    Inflammatory Response

    • Leukocytes and plasma proteins are crucial components of the inflammatory response.
    • Inflammatory sites have increased blood flow into tissue, leukocyte adhesion to endothelial lining of venules, and changes in vascular permeability.

    Function of Macrophages

    • Macrophages are crucial parts of the inflammatory response. (They can be activated by cytokines.)
    • Macrophage activation leads to enhanced inflammation and killing of microbes. Cytokines like TNF, IL-1, IL-6, IL-12, initiate and regulate macrophage activity, leading to the removal of pathogens.

    Local and Systemic Actions of Cytokines

    • Cytokines such as TNF, IL-1, IL-6, and chemokines drive the inflammatory response locally as well as systemically.
    • Systemically, cytokines (e.g., TNF, IL-1, IL-6) cause changes like fever and increased acute-phase protein production.

    Hypersensitivity

    • Pathogenic immune reactions lead to hypersensitivity of various types. Immediate hypersensitivity reactions (Type I) are IgE-mediated reactions leading to mast cell activation.

    Pathogenesis of immune complex Diseases in Kidneys

    - Complexes containing cationic antigens.
- Complex deposits in sites where plasma is ultra-filtered

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    Immune Response in Kidney Disease PDF

    Description

    Test your knowledge on chronic inflammation, types of hypersensitivity reactions, and the roles of various immune cells and complement components. This quiz covers key concepts and functions related to the immune response and inflammatory processes.

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