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Summary - Lectures

  • 1 Re-visiting our immune system; Adaptive immunity:immune cells and immune regulation

  • What is the role of the immune system?
    Defense against invading pathogens
  • Name the three "organs" of the immune system:
    Mechanical bariers
    Blood circulation
    Lymphe circulation
  • What is the mechanical barrier of the immune system?
  • What is important for the blood circulation, regarding the immune system?
    Bone marrow
  • What is important for the lymphe circulation, regarding the organs of the immune system?
    Thymus, lymph nodes, Specialized lymphoid structures located in a variety of organs: e.g. MALT (mucosa-associated lymphoid tissue)

  • Where can you find monocytes?
    Monocytes circulate in the blood. When monocytes reside in tissue they differentiate into either immature DC or macrophages.
  • What does a natural killer cell do?
    Kills cells infected with certain viruses
  • What does a neutrophil do?
    Phagocytosis and killing of microorganisms
  • What does an eosinophil do?
    Kills antibody-coated parasites through release of granule contents
  • What does a DC do?
    activates T-cells and initiates adaptive immune response
  • What does a mastcell do?
    Expulsion of parasites from body through release of granules containing histamine and other active agents
  • What does a monocyte do?
    circulates, precursor cell to marcophage
  • What does a macrophage do?
    phagocytosis and killing of microorganisms. Activation of T cells and initiation of immune responses
  • What does a small lymphocyte do?
    produces antibodies (b cells) or cytotoxic and helper functions (T cells)
  • What is and does a plasma cell do?
    Fully differentiated form of B cell that secretes antibodies
  • What is characteristic for the innate immune responses?
    not very specific
  • What is characteristic for the adaptive immune responses?
    self/ non-self
  • Name the three big steps in defense against pathogens:
    1) Alarm and first defense- aspecific killing (“quick and dirty”)- local inflammation
    2) Mobilisation of the immune system- recruitment of immune cells- activation of adaptive responses -> antigen presentation !!
    3) Specific defence & future protection- clonal selection of lymphocytes- effector B(plasma)-cells and T-cells- memory

  • Explain what happens in local inflammation
    1) healty skin is not inflamed
    2) surface wound introduces bacteria, which activate resident effector cells to secrete cytokines
    3) vasodilation and increased vascular permeability allow fluid, protein and inflammatory cells to leave blood and enter tissue
    4) the infected tissue becomes inflamed, causing redness, heat, swelling and pain.

  • Explain what happens to neutrophils from bone marrow till death
    1) large reserves of neutrophils are stored in the bone marrow and are released when needed to fight infection
    2) neutrophils travel to and enter the infected tissue, where they engulf and kill bacteria. The neutrophils die in the tissue and are engulfed and degraded by Macrophages
  • Explain how complement gets activated
    1) Bacterial cell surface induces cleavage and activation of complement.
    2) One complement fragment covalently bonds to the baterium, the other attracts an effector cell.
    3) The complement receptor on the effector cell binds to the complement fragment on the bacterium
    4) the effector cell engulfs the bacterium, kills it and breaks it down.
  • How do macrophages initiate immune responses? Explain
    Macrophages initiate immune responses by activating T-cells. 
    1) Bacteria binding to endocytic receptors of macrophages induce their engulfment and degration
    2) baterial components binding to signaling receptors of macrophages induce the synthesis of inflammatory cytokines
  • How do T cells activate macrophages?
    1) Bacterial peptides transported by MHC class II to the cell surface
    2) Th1 cell recognizes complex of peptide antigen with MHC class II and activated macrophage 
  • What does the B cell receptor recognize?
    complex antigenic structures
  • What does the T cell receptor recognize?
    small peptide fragments (requires antigen presentation) 
  • How are B cell receptors activated?
    By crosslinking with antigens
  • What is clonal selection?
    Multiplication of specific lymphocytes
  • What is required for T-cell activation?
    2 signals: co-stimulatory signal and specific signal
    Specific signal alone leads to an anergic T ceel, this contributes to self-tolerance
    Co-stimulatory signal alone has no effect on the T cell
  • What kind of T cells do you have?
    CD8+  cytotoxic T-cells (Tc )
    CD4+  helper T-cells of type 1 (Th1)
    CD4+  helper T-cells of type 2 (Th2)
    Regulatory T-cells
  • CD8 T-cell + virus-infected cell =
    dead virus infected cell
  • CD4 Th1 cell + macrophage =
    cytokines for CD4 Th1 cell, CD4 Th1 cell activates macrophage
  • CD4 Th2 cell + B cell =
    cytokines to B cell --> plasma cell (producing antibodies)
  • What is the action of CD8 cytotoxic t cells?
    1) virus infects cell
    2) virus proteins synthesized in cytoplasm
    3) peptide fragments of viral proteins bound by MHC class I in ER
    4) bound peptides transported by MHC class I to the cell surface
    5) cytotoxic T cell recognizes complex of viral peptide with MHC class I and kills infected cell
  • Which MHC class is involved in CD8 T cells?
  • What is the action of CD4 Thelper cells? (Th1+Th2)
    1) Marcophage engulfs and degrades bacterium, producing peptides
    2) Bacterial peptides bound by MHC class II in vesicles
    3) Bacterial peptides transported by MHC class II to the cell surface
    4) Th1 cell recognizes complex of peptide antigen with MHC class II and activates macrophage

    1)Cell-surface immunoglobulin of B cell binds bacteria and engulfs and degrades them, producing peptides
    2) bacterial peptides bound by MHC class II in vesicles
    3) Bound peptides transported by MHC class II to the cell surface
    4) Th2 cell recognizes complex of peptide antigen with MHC class II and activated B cell
  • What is the difference in antigen presentation between MHc class I and II?
    Class I has internal foreign protein, while class II has external foreign protein
  • What are the T cell effector molecules of the CD8 cytotoxic T cell?
    Perforin, Granzymes, Granulysin, Fas ligand
    Others: IFN-gamma, TNF- beta, TNF-alpha
  • What are the T cell effector molecules of the CD4 Th1 cell?
    IFN-gamma, GM-CSF, TNF-alpha, CD40 ligand, Fas ligand
    Others: IL-3, TNF-beta, (IL-2)
  • What are the T cell effector molecules of CD4 Th2 cells?
    IL-4, IL-5, IL-15, CD40 ligand
    Others: IL-3, IL-10, GM-CSF, TGF-beta, Eotaxin
  • The inhibitory signals distributed by a Th2 cell are ... and the function is ..
    IL-4, 10, 13.Inhibition on Th1 and macrophages
  • What are the signals that let Th1 cells inhibit Th2?
    IFN-gamma, TNF-alpha
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50B) Infections can cause the break down or tolerance to self-antigens by several mechanisms, which result in the onset of autoimmunity. b. Describe in detail one mechanism that is based on pathogen-specific antigen(s) (also known as “molecular mimicry”) (4p)
Pathogens may contain antigenic structures or peptides that resemble self antigen(s). When pathogen-activated T and B cells specific for those antigens cross-react with the respective self antigens an autoimmune reaction occurs. When conditions favor the further activation of these cross-reactive T or B cells, an autoimmune disease can develop. 
50 c. Describe in detail one mechanism that is not based on pathogen antigen-specificity (i.e., bystander activation) (4p) 
Chronic infection ! long term inflammation leads to tissue damage and enhanced MHC-class II expression on non-phagocytic cells (due to high concentrations of INF-γ) which in combination favor presentation of autoantigens. 
Autoreactive T cells that have escaped from negative selection in the thymus can become activated under these conditions. 
Bystander activation of autoreactive T cells ! In a strong inflammatory environment (because of an immune response to any antigen) Regulatory T cells that usually prevent activation of may become “overruled” and subsequent activation of autoreactive T cells may occur. 
Question 50. Epidemiological data suggest that infections may play a role in – or increase the risk of developing (an) autoimmune disease(s). a. Give two reasons why it is difficult to prove that a specific infection is the cause of a particular autoimmune disease. (2 ptn) 
- AID develop gradually and often over a long period of time. Usually, the pathogens that initiated or accelerated this process are not present anymore (eradicated by the  immune system) 
 - There is no 1 to 1 association between pathogens and the autoimmune diseases that they are thought to play a role in (a particular pathogen may induce different autoimmune diseases or a particular autoimmune disease may be caused by different pathogens).
49 d. Name two antigenic properties/circumstances that increase the ability of an antigen to induce immunological tolerance (2 points) and explain for each property the  mechanism by which tolerance is induced. (2 points) 
1. Presence: constitutive presence during maturation of lymphocytes > clonal deletion of lymphocytes 
2. Dose: high/low dose > anergy (immunological deafness) 
3. Route: in particular, oral contact > suppression 
4. antigen-presentation: lack of co-stimulation leads to anergy
Autoimmune diseases arise when the tolerance for self-antigens is broken. A healthy immune system is not only tolerant for self-antigens, but also for many other antigens. 49 c. Give a precise definition of “immunological tolerance”. (2 points) 
Immunological tolerance is the suppression of immune response(s) agains a 
specific antigen because of previous exposure to that particular antigen. 
(So immunological tolerance is based on memory!) 
49 b. Explain why, in theory, every individual has the ability to develop an autoimmune disease. (2 points)
In each single individual B- and T cells are being randomly generated in order to 
recognize as much as possible different antigens, so many premature lymphocytes develop receptors that bind to self antigens.  
When such auto reactive T cells escape negative selection in the thymus and enter the periphery they may become activated under specific circumstances. Conditions that favor the activation of T cells include release of autoantigens due to physical damage, an excess of inflammatory mediators due to chronic inflammation or infection and/or breakdown of peripheral tolerance /regulatory T cells. 
Question 49. a. Explain the difference between auto-reactivity and autoimmune disease (2 points)
Autoreactivity: recognition/binding of T- or B-cell receptors to self 
antigens in the absence of symptoms. 

Autoimmune disease: autoreactivity that causes disturbance of physiological 
processes or damage, resulting in symptoms/disease. 
Question 48. Hypersensitivity reactions can be categorized into Type I, II, III and IV reactions. a. Name one drug or substance that can induce a Type II hypersensitivity. (2 points) b. What is the name of the disease that is caused by this drug/substance? (2 points) c. Explain in detail the mechanism by which drugs can trigger type II hypersensitivity reactions (6 points)
Chemically reactive drugs such as penicillin, quinidine or methyldopa 
Causing haemolytic anaemia or thrombocytopenia, respectively 
Chemically reactive drugs such as penicillin, quinidine and methyldopa bind to 
surface components of erythrocytes or platelets and generate novel „foreign‟ epitopes to which the immune system is not tolerant. The host mounts an IgM or IgG response to these epitopes. Complement is activated, bringing about the destruction of erythrocytes or platelets through the formation of the membrane-attack complex and/or opsonization, causing hemolytic anemia or thromobocytopenia, respectively
47. Regulatory T cells do not express a. CD25 b. AIRE c. FoxP3 d. CTLA-4
46. Graves‟ disease causes , whereas Hashimoto‟s disease causes . a. hypothyroidism; hyperthyroidism b. hyperthyroidism; hypothyroidism c. hypoglycemia; hyperglycemia d. hyperglycemia; hypoglycaemia