Term
| What are toll-like receptors? Describe them. |
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Definition
| receptors that can be cell-surface receptors which can recognize teichoic acid, which is found on the surface of gram negative bacteria, or they can be intracellular receptors that sense intracellular bacteria; they have leucine-rich domains and mammals have some 10 different toll-like receptors |
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Term
| Which is the first responder: innate or acquired immunity? How do they differ? |
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Definition
1. innate immunity
2. innate immunity is nonspecific, consisting of things like skin, acid, mucosa, phagocytic cells, destructive compounds, and natural killer cells; acquired immunity are developed specifically against some antigen and consist of humoral immunity (circulating and mucosal antibodies) and cell-mediated immunity (consisting of activated cells) |
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Term
| What is the acquired immune system composed of? |
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Definition
| B cells, antigen-presenting cells, T cells |
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Term
| What kinds of T cells are there (that you have to learn about)? Which is the most common? |
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Definition
1. T helper cells (CD4+), cytotoxic T cells (CD8+), and T regulatory cells (CD4+ and CD25+)
2. T helper cells |
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Term
| How is the adaptive immune system able to produce so much variety of T cell receptors and antibodies? |
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Definition
| it is able to shuffle gene expression for both to produce billions of combinations |
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Term
| What is the sequence of events involved in activation of the adaptive immune response? |
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Definition
a. inactive lymphocytes
b. invasion of body by foreign antigen
c. phagocytosis by macrophages
d. presentation of antigen to lymphocytes |
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Term
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Definition
1. a substance that can induce an immune response when introduce into an immunocompetent host and that can react with the antibody produced from that response; usually a macromolecule with recurring molecular structure like a polysaccharide or a protein
2. a regular recurring molecular group, which the immune system uses are a signal for immune response |
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Term
| What do immunologists mean when they say lymphocytes are "educated"? |
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Definition
| after differentiating in the bone marrow, lymphocytes are tested for reactivity and self-reactivity; non-reactive and self-reactive lymphocytes are destroyed before they can become active; B cells are "educated" in the bone marrow and T cells are "educated" in the bone marrow and then against in the lymphoid tissue (thymus) |
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Term
| What is the function of regulatory T cells? |
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Definition
| they prevent T4 helper cells and cytotoxic cells from becoming too reactive |
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Term
| What happens when a naïve cell is first exposed to an antigen? What happens when the body encounters that antigen again? |
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Definition
1. some memory cells are produced and a few activated cells are eventually produced
2, more memory cells are produced and a host of activated cells are produced |
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Term
| How do memory B and memory T cells compare? |
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Definition
| memory B cells assist with stronger antigen binding and memory T cells are involved in the production of cytokines to fight the invading antigen |
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Term
| What happens when a lymphocyte is discovered to be self-reactive in the lymphoid tissue? What if it is discovered to be self-reactive in circulation? |
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Definition
1. it is either inactivated or destroyed
2. an autoimmune disease develops |
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Term
| How is the production of antibodies initiated? |
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Definition
| lymphocytes with various receptors are made; when an antigen show up and activates one of the the receptors, the cell produces 2000 antibodies per second for several days to fight the antigen... then dies |
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Term
| Why can multiple antigens be produced for the same invading substance/organism? |
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Definition
| the substance/organism may have multiple determinants; each determinant can have one antibody developed for it |
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Term
| What are the classes of antibodies? How do they vary and how are they similar? |
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Definition
IgA - found in secretions, saliva, respiratory tract, and GI tract secretions
IgD - binds to mas and basophils; stimulates these cells to release antimicrobial substances
IgE - binds to mast cells; secreted as an allergic response
IgG - major Ig in the blood
IgM - secreted first; have 10 binding sites
They are all similar in that they can all have the same binding region; however, their constant region differs from one another |
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Term
| What are the parts of an antibody structure? |
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Definition
| the antigen-binding site (Fab fragment) and the constant site (Fc fragment); the Fab fragment consists of two heavy medial chains attached to two light lateral chains, both of which are attached to the Fc fragment by the hinge region |
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Term
| Where do naïve lymphocytes reside until they are activated? |
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Definition
| in lymphoid tissue, such as the spleen or lymph node |
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Term
| How can we create vaccines that cause a greater immune response to viruses that our bodies do not react very strongly to? |
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Definition
| our bodies will not react strongly if the virus contains a region that is similar to "self" proteins; we can develop a vaccine against this virus by making the vaccine contain the non-self region of the virus and a vastly different protein (a "slug protein" for example) |
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Term
| Why is myelin sometimes targeted for destruction by the immune system? |
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Definition
| it has a repeating sequence, which initially appear antigenic to the immune system |
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Term
| What happens when a B-cell is influenced by a T4 helper cell? |
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Definition
| T4 helper cells can activate B cells; the B cells can differentiate into a plasma cells and produce IgG antibodies; each IgG antibody produced by a given B cell attaches to the same receptor |
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Term
| How many different antibodies are thought to be in our bodies at a given time? How many are we thought to develop in our lives? |
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Definition
1. about 100 million
2. about 10 billion |
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Term
| How many variations in VDJC genes can code for the following: light chains, heavy chains? |
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Definition
1. 30-40 in V, 4-5 in J
2. 51 in V, 27 in D, 6 in J |
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Term
| How many variations in VDJC genes can code for the following: TCR α, β, γ, δ? |
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Definition
1. 50 in V, 70 in J
2. 57 in V, 2 in D, 13 in J, 2 in C
3. 14 in V, 5 in J
4. 3 in V, 3 in D, 3 in J, 1 in C |
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Term
| What common genes are varied to provide diversity in immune system responses (especially in TCR)? |
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Definition
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Term
| What is the complement complex? |
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Definition
| a system in the innate immune system consisting of 20 proteins that can be activated in various ways to destroy bacteria |
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Term
| What is humoral immunity? Cell-mediated immunity? |
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Definition
1. immunity involving the release of antibodies into circulation by B cells
2. immunity involving T cells that are specifically designed to fight one type of antigen |
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Term
| How are macrophages involved in lymphocyte activation? |
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Definition
| macrophages mostly digest antigens and then can present part of the antigen to lymphocytes to activate the lymphocytes |
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Term
| What are the classes of antibodies? |
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Definition
| IgM, IgG, IgA, IgD, and IgE |
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Term
| What is the most common antibody? Which acts as the primary response? Which acts against allergies? |
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Definition
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Term
| In what ways can antibodies disable an antigen by direct attack? How can antibodies disable antigens by indirect attack? |
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Definition
1. a. agglutination
b. precipitation
c. neutralization
d. lysis
2. activation of the complement proteins |
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Term
| For complement proteins, what is the function of C3? C5? |
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Definition
1. opsonization (labeling antigens for phagocytosis)
2. is cleaved into C5b and C5a; C5a is involved in chemotaxis of WBCs and activate mast cells and basophils; C5b starts the later cascade that forms the attack complex |
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Term
| For complement proteins, what is the function of C3a? C4a? C5a? |
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Definition
| they all recruit mast cells and basophils (chemotaxis) to initiate cell degradation via histamine, meaning some smooth muscle contraction, increased vasodilation, and increased vascular permeability (to allow phagocytes through the blood vessels to attack the bacterium) |
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Term
| Which complement proteins are involved in forming the attack complex? |
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Definition
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Term
| What are the methods by which complement proteins can be activated? Describe them. |
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Definition
a. classical pathway - antibody dependent activation
b. mannose pathway - antibody-independent; lectin binds to carbohydrates on bacteria
c. alternative pathway - anti-body independent |
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Term
| Why is the mannose pathway for complement proteins useful? |
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Definition
| lipopolysaccharide resides in the cell membranes of gram- bacterial; this molecule has large amounts of mannose, which will activate the pathway |
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Term
| What measures exist to prevent complement proteins from destroying the body? |
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Definition
a. the proteins are labile (easily disabled by heat)
b. they become inactivated as they get farther from their targets
c. negative regulators of complement proteins exist in the plasma |
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Term
| What congenital complement protein disorders exist and what are the consequences of the disorders? |
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Definition
a. a lack of C1, C4, and C2 (-/-) - patients are prone to immune complex diseases and constant inflammation (lupus, glomerulonephritis, and vasculitis)
b. Factor D (-/-) - increased nesseria infections
c. Lack of C3 - patients are prone to sever and persistent bacterial infections |
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Term
| What if the function of the attack complex? |
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Definition
| it can form large pores in invading bacterial membranes; these pores can drain the cells of cytoplasm and the cells will die |
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Term
| What are the kinds of T cells (that we need to know)? |
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Definition
| cytotoxic T cells (CD8), regulatory T cells (CD4 and CD25), and helper T cells (CD4) |
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Term
| What is the function of T helper cells? |
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Definition
| they release lymphokines that activate B lymphocytes and cytotoxic T cells; once the T lymphocytes are activated, they can activate B lymphocytes, causing them to turn into active plasma cells |
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Term
| How do the functions of helper T cells, regulatory T cells, and cytotoxic T cells vary? |
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Definition
| cytotoxic T cells recognize foreign particles on foreign cell surfaces and attack those cells; helper T cells recognize foreign particles that are presented by antigen-presenting cells via MHC II and then release lymphokines to activate other lymphocytes; regulatory T cells prevent cytotoxic T cells from getting out of control |
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Term
| What are the major types of antigen-presenting cells? Which is the most potent? |
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Definition
1. dendritic cells, B lymphocytes, and macrophages
2. dendritic cells |
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Term
| How are T-cells activated? |
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Definition
| the T-cell's cell adhesion molecule interacts with an antigen-presenting cell's cell adhesion molecule and the antigen-presenting cell presents an anitgen with the MHC receptor to the T cell's T-cell receptor, activating it; helper T cells also need exposure to IL-1 or a membrane-bound molecule |
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Term
| What is the difference in MHC I and II in terms of function? |
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Definition
a. MHC I receptors are present on all self cells and present self and foreign proteins that are present inside the cell; cytotoxic T cells will interact with these MHC I receptors and recognize a self antigen and attack when a foreign antigen is present
b. MHC II receptors present antigens to helper T cells to activate them |
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Term
| Which antibody can cross the placenta? Which can bind to macrophages and neutrophils? Which can bind to mast cells and basophils? Which activates the complement system? |
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Definition
1. IgG
2. IgG
3. IgE
4. IgG and IgM (IgM is more powerful in this action) |
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Term
| What is the function of interferon γ? Where is it secreted from? |
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Definition
1. sometimes viruses and tumor cells mask their presence by disabling the MHC I receptors that would present their antigens; interferon γ resists the disabling process of MHC I and increases its expression
2. T helper cells |
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Term
| What is the process of T cell activation when a dendritic cell comes into contact with an antigen? |
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Definition
| the denritic cell, having come into contact with an antigen, leaves the local tissue and goes into the lymph node to activate naïve T helper cells; after it does so, the cells undergo cell division and create effector cells and memory cells |
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Term
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Definition
| the increase of effector and memory cells due to only a few activated T helper cells |
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Term
| What is the significance of IL-2? IL-4? IL-5? IL-6? |
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Definition
1. it has a strong influence on the growth and proliferation of other T lymphocytes; it can also work in a paracrine or autocrine manner
2-4. a strong stimulation for B-cell growth |
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Term
| What chemicals can T cells produce to assist with immune cell activation? |
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Definition
| IL-2, IL-3, IL-4, IL-5, IL-6, interferon γ, and GM-CSF |
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Term
| What happens when a cytotoxic cell recognizes an antigen on an MHC I receptor as a foreign antigen? |
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Definition
| it can bind to the infected cell, induce the antigen-presenting cell to kill itself, or punch holes in the cell membrane with perforins |
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Term
| What is the difference between active and passive immunity? |
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Definition
| active immunity is when the body develops an immunity against an invading virus, bacterium, or antigen; passive immunity is when the antibodies or T cells of someone else are transfused into the patient's body, so the patient has an acquired immunity that he himself did not originally acquire |
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Term
| Describe: Fas and fas ligand |
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Definition
| Fas is a membrane-bound receptor that is found on the surfaces of some pathogens and the Fas ligand is found on the surface of cytotoxic T cells; the binding of the Fas ligand to Fas causes the activation of the Fas death domains, which activates caspases and causes cells to undergo apoptosis; it is especially important that there is no interaction between Fas and Fas ligands in transplant situations |
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Term
| What is the function of NK cells? |
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Definition
| natural killer cells; they use killer inhibitor receptors (KIRs), which sense whether or not a cell has MHC I receptors; if MHC I receptors are present, the KIRs are activated; if the MHC I is present, the KIRs are inactivated and the NK cells begin non-specific killing, inducing apoptosis in the cell |
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Term
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Definition
| an antigen that reacts with a specific type of IgE reagin to cause an immune response |
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Term
| Describe: delayed-type hypersensitivity allergy. |
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Definition
| a localized inflammatory response to an allergen; this allergic response is due to a reaction between an allergin and an IgE reagin; IgE can bind to mast cells and basophils and, when they interact with the allergen, can cause the basophils and mast cells to rupture, releasing tons of cytokines into the plasma (which can cause inflammation, vasodilation, and a host of symptoms depending on the tissue); some of the chemicals released are also chemotaxis factors that recruit eosinophils and neutrophils to the area of reaction |
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Term
| What is the mechanism for onset of anaphylaxis? How does one stop this? |
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Definition
1. when an allergen is introduced to mast cells and basophils in circulation, it causes the rupture of mast cells and basophils, resulting in large amounts of histamine being released; the histamine can cause body-wide vasodilation and increased blood vessel permeability, resulting in shock; mast cells and basophils will also release (among other things) slow-reacting substance of anaphylaxis, which can cause spasms in the smooth muscle of bronchioles, elliciting an asthma attack
2. epinephrine to oppose the histamine |
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Term
| What is urticaria? What is the mechanism of its onset? How is it treated? |
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Definition
1. hives
2. an antigen entering specific skin area activates a localized anaphylactoid reaction; histamine causes vasodilation and a red flare and increased permeability of the blood vessels, resulting in swelling in areas of the skin, referred to as hives
3. anti-histamines can prevent the hive formation and reduce the redness, etc |
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Term
| What is hay fever? What is the mechanism of its onset? |
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Definition
1. an allergen-reagin reaction occurring inside the nose
2. the allergen-reagin reaction causes the release of histamine, which results in intranasal dilation with increased capillary pressure and increased capillary permeability; this causes rapid fluid leakage into the nasal cavities and deeper tissues of the nose; other linings become swollen and secretory and other products of the allergen-reagin reaction can cause irritation in the nose, resulting in sneezing
3. anti-histamines can reduce this reaction |
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Term
| What is the onset of allergy-induced asthma? How is it treated? |
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Definition
1. the allergen-reagin reaction results in the release of slow-reacting substance of anaphylaxis, which causes bronchospasms, resulting in asthma
2. anti-histamines are NOT effective because the reacting chemical involved is not histamine; epinephrine or other bronchodilators will be effective |
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Term
| What is hypersensitivity in allergies? What are its different types? |
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Definition
1. a systemic response in reaction to an allergen
2. a. type I - anaphylactic (shock-inducing)
b. type II - blood-transfusion reactions (ex. megaloblastic fetalis)
c. type III - auto-immune diseases
d. type IV - organ transplant rejection |
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Term
| How are atopic allergies spread? |
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Definition
| they are genetically set and environmentally activated |
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